[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"_public_publisher_byId_4cd68f35-4ac6-4047-8542-743353c89591":3,"_public_publication_all{\"sortAscending\":false,\"sortField\":\"updateTime\",\"page\":0,\"size\":10,\"facet\":true,\"searchKey\":\"publisherId:4cd68f35-4ac6-4047-8542-743353c89591,\"}":97},{"code":4,"data":5,"meta":20},"SUCCESS",{"id":6,"createTime":7,"updateTime":8,"relativeEntities":9,"slug":10,"properties":11,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":22,"manageAffiliations":35,"indexDatabases":50,"url":20,"thumbnailPath":20,"statistic":87,"gsStatistic":20,"type":96,"analyzePriority":20},"4cd68f35-4ac6-4047-8542-743353c89591","2024-04-08T00:23:34.069+00:00","2025-11-21T09:47:28.591+00:00",[],"Immunity-Ageing",{"issn":12,"title":14,"url":16},{"VOID":13},"17424933",{"EN":15},"Immunity & Ageing",{"VOID":17},"https:\u002F\u002Flink.springer.com\u002Fjournal\u002F12979","PUBLISHER","PENDING",null,0,[23,29],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":25,"label":26,"description":28,"parentId":20,"standard":20,"scholarHubFieldId":20},"b2f3603d-283c-49e1-a8f1-01f0de24243c",[],{"EN":27},"Immunology",{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":31,"label":32,"description":34,"parentId":20,"standard":20,"scholarHubFieldId":20},"d76fbb41-9ab4-4d15-9c02-a6f9918892d8",[],{"EN":33},"Aging",{},[36,43],{"id":37,"createTime":20,"updateTime":20,"relativeEntities":38,"slug":20,"properties":39,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":42,"statistic":20},"c5894808-4e99-4047-bbce-594f58821845",[],{"title":40},{"EN":41},"BioMed Central Ltd.",[],{"id":44,"createTime":20,"updateTime":20,"relativeEntities":45,"slug":20,"properties":46,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":49,"statistic":20},"67883518-0c98-470e-b6b0-160ab49bb03d",[],{"title":47},{"EN":48},"BMC",[],[51,69],{"id":52,"indexDatabase":53,"url":63,"indexYears":64,"academicFieldIds":65,"indexDatabaseRanking":68},"a632b04e-a911-42a1-865e-bd3361250da5",{"id":54,"createTime":20,"updateTime":20,"relativeEntities":55,"label":56,"description":58,"key":60,"publicationTags":61,"standard":20},"3c7051d4-eb7d-4c57-a56b-36fc74c5d1e9",[],{"EN":57,"VI":57},"Scopus - Elsevier",{"EN":57,"VI":59},"Cơ sở dữ liệu Scopus thuộc Elsevier","scopus",[62],"SCOPUS","https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002F4400151516","2004-2025",[66,67],"2e85ca04-4b9c-4f3e-be83-f6e278d9077d","5b1a613c-f8d0-45b5-8ad0-681d8cd14875","SCOPUS__Q2",{"id":70,"indexDatabase":71,"url":83,"indexYears":20,"academicFieldIds":84,"indexDatabaseRanking":20},"dfd6cb57-9748-452d-8116-f59f2451500c",{"id":72,"createTime":20,"updateTime":20,"relativeEntities":73,"label":74,"description":76,"key":79,"publicationTags":80,"standard":20},"a4921856-b128-4d9f-8f1f-e80813d3bbd4",[],{"EN":75,"VI":75},"ISI\u002FSCIE - Science Citation Index Expanded",{"EN":77,"VI":78},"SCIE database","Cơ sở dữ liệu SCIE","scie",[81,82],"SCIE","ISI","https:\u002F\u002Fmjl.clarivate.com\u002Fsearch-results?issn=1742-4933",[85,86],"03744874-dcbd-436b-8d5c-f6fa955ce005","944e9ce4-ecc3-447c-87ab-6db4438ce104",{"impactFactor":21,"impactFactorByYear":88,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":89,"totalPublicationByYear":90,"totalCitation":21,"totalCitationByYear":94,"totalCitationPerPublication":21,"totalCitationPerPublicationByYear":95,"hindexLast5Year":21,"hindex":21},{},16,{"2005":91,"2010":91,"2014":92,"2020":92,"2022":92,"2023":91,"2024":93},1,2,7,{},{},"JOURNAL",{"meta":98,"data":100},{"total":99},"394",[101,203,704,896,1068,1554,1730,1815,1965,2386],{"id":102,"createTime":103,"updateTime":104,"relativeEntities":105,"slug":106,"properties":107,"entityType":118,"verifyStatus":119,"verifyTime":120,"verifyNote":121,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":122,"fullTextUrl":20,"authors":123,"publicationType":140,"publisherRelationship":141,"citationCount":192,"citationInfo":193,"publishDate":199,"publishYear":194,"citationAnalyzeStatus":19,"lastCitationAnalyze":200,"indexDatabases":201,"openAccess":20,"references":20,"isForceReanalyzing":202},"bb542f22-9765-4dc0-8122-714466fd55b8","2024-01-19T04:09:26.503+00:00","2026-07-20T21:58:34.908+00:00",[],"Ageing-and-the-immune-system-in-vivo-commentary-on-the-16th-session-of-British-Society-for-Immunology-Annual-Congress-Harrogate-December-2004",{"abstract":108,"title":110,"gsPaper":112,"references":114,"doi":116},{"EN":109},"The problems associated with the ageing immune system coupled with possible solutions were discussed recently at the British Society for Immunology Annual Congress in Harrogate in December 2004. The session \"Ageing and the Immune System in vivo\" dealt in details with the immune risk phenotype and the potential methods of reversing the problems of an ageing immune system. This is a commentary on that session.",{"EN":111},"Ageing and the immune system in vivo: commentary on the 16th session of British Society for Immunology Annual Congress, Harrogate, December 2004",{"VOID":113},"[\"9156179825632060980\"]",{"VOID":115},"Aspinal R: Age-related changes in the function of T cells. Microsc Res Tech. 2003, 62: 508-513. 10.1002\u002Fjemt.10412.\nAspinal R: Longevity and the immune response. Biogerontology. 2000, 1: 273-278. 10.1023\u002FA:1010046532657.\nPawelec G, Akbar A, Caruso C, Effros R, Grubeck-Loebenstein B, Wikby A: Is immunosenescence infectious?. Trends Immunol. 2004, 25: 406-410. 10.1016\u002Fj.it.2004.05.006.\nPawelec G, Barnett Y, Forsey R, Frasca D, Globerson A, McLeod J, Caruso C, Franceschi C, Fulop T, Gupta S, Mariani E, Mocchegiani E, Solana R: T cells and aging. January 2002 update. Front Biosci. 2002, 7: d1056-d1183.",{"VOID":117},"10.1186\u002F1742-4933-2-5","PUBLICATION","VERIFIED","2024-05-28T17:16:36.593+00:00","Auto Verify","https:\u002F\u002Fimmunityageing.biomedcentral.com\u002Farticles\u002F10.1186\u002F1742-4933-2-5",[124],{"id":125,"sortIndex":21,"researcher":20,"roles":126,"affiliations":128,"properties":137,"displayName":139,"givenName":20,"familyName":20},"5185e7b2-b5df-4cc6-8b83-9a0c64c93780",[127],"AUTHOR",[129],{"id":130,"sortIndex":21,"affiliation":131,"properties":20},"17f227cf-a634-4eaf-b7cd-9e9173d87163",{"id":130,"createTime":20,"updateTime":20,"relativeEntities":132,"slug":20,"properties":133,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":136,"statistic":20},[],{"title":134},{"VI":135},"Dept of Immunology, Imperial College London, Chelsea & Westminster Hospital London, London, UK",[],{"title":138},{"VI":139},"Richard Aspinall","ARTICLE",{"url":122,"publisher":142,"properties":187},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":143,"slug":10,"properties":144,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":147,"manageAffiliations":156,"indexDatabases":167,"url":20,"thumbnailPath":20,"statistic":182,"gsStatistic":20,"type":96,"analyzePriority":20},[],{"issn":145,"title":146},{"VOID":13},{"EN":15},[148,152],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":149,"label":150,"description":151,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":153,"label":154,"description":155,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":33},{},[157,162],{"id":37,"createTime":20,"updateTime":20,"relativeEntities":158,"slug":20,"properties":159,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":161,"statistic":20},[],{"title":160},{"EN":41},[],{"id":44,"createTime":20,"updateTime":20,"relativeEntities":163,"slug":20,"properties":164,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":166,"statistic":20},[],{"title":165},{"EN":48},[],[168,175],{"id":52,"indexDatabase":169,"url":63,"indexYears":64,"academicFieldIds":174,"indexDatabaseRanking":68},{"id":54,"createTime":20,"updateTime":20,"relativeEntities":170,"label":171,"description":172,"key":60,"publicationTags":173,"standard":20},[],{"EN":57,"VI":57},{"EN":57,"VI":59},[62],[66,67],{"id":70,"indexDatabase":176,"url":83,"indexYears":20,"academicFieldIds":181,"indexDatabaseRanking":20},{"id":72,"createTime":20,"updateTime":20,"relativeEntities":177,"label":178,"description":179,"key":79,"publicationTags":180,"standard":20},[],{"EN":75,"VI":75},{"EN":77,"VI":78},[81,82],[85,86],{"impactFactor":21,"impactFactorByYear":183,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":89,"totalPublicationByYear":184,"totalCitation":21,"totalCitationByYear":185,"totalCitationPerPublication":21,"totalCitationPerPublicationByYear":186,"hindexLast5Year":21,"hindex":21},{},{"2005":91,"2010":91,"2014":92,"2020":92,"2022":92,"2023":91,"2024":93},{},{},{"pages":188,"volume":190},{"VOID":189},"1-2",{"VOID":191},"2",43,{"total":192,"publishYear":194,"statisticByYear":195},2005,{"2005":91,"2006":92,"2007":196,"2008":91,"2009":91,"2010":91,"2011":197,"2012":92,"2013":91,"2014":92,"2016":197,"2017":196,"2018":91,"2019":196,"2021":197,"2022":198,"2023":92,"2024":91},4,3,6,"2005-02-22","2026-07-20T21:58:34.907+00:00",[68,81],false,{"id":204,"createTime":205,"updateTime":206,"relativeEntities":207,"slug":208,"properties":209,"entityType":118,"verifyStatus":119,"verifyTime":220,"verifyNote":121,"languages":20,"translateLanguages":20,"viewCount":92,"primaryUrl":221,"fullTextUrl":20,"authors":222,"publicationType":140,"publisherRelationship":650,"citationCount":20,"citationInfo":20,"publishDate":701,"publishYear":702,"citationAnalyzeStatus":19,"lastCitationAnalyze":206,"indexDatabases":703,"openAccess":20,"references":20,"isForceReanalyzing":202},"d29e43f5-046c-4a44-814f-e703ed3a41f8","2023-12-04T18:17:47.511+00:00","2026-07-07T05:45:24.833+00:00",[],"Short-term-intensive-fasting-enhances-the-immune-function-of-red-blood-cells-in-humans",{"abstract":210,"title":212,"gsPaper":214,"references":216,"doi":218},{"EN":211},"Fasting is known to influence the immune functions of leukocytes primarily by regulating their mobilization and redistribution between the bone marrow and the peripheral tissues or circulation, in particular via relocalization of leukocytes back in the bone marrow. However, how the immune system responds to the increased risk of invasion by infectious pathogens with fewer leukocytes in the peripheral blood during fasting intervention remains an open question. We used proteomic, biochemical and flow cytometric tools to evaluate the impact of short-term intensive fasting (STIF), known as beego, on red blood cells by profiling the cells from the STIF subjects before and after 6 days of fasting and 6 days of gradual refeeding. We found that STIF, by triggering the activation of the complement system via the complement receptor on the membrane of red blood cells, boosts fairly sustainable function of red blood cells in immune responses in close relation to various pathogens, including viruses, bacteria and parasites, particularly with the pronounced capacity to defend against SARS-CoV-2, without compromising their oxygen delivery capacity and viability. STIF fosters the immune function of red blood cells and therefore, it may be considered as a nonmedical intervention option for the stronger capacity of red blood cells to combat infectious diseases. STIF fosters the immune response of red blood cells to various pathogens, in particular SARS-CoV-2, via activation of the complement receptor on their membranes. STIF does not compromise the oxygen transport capacity or viability of red blood cells. \n                  \n                    \n                  \n                ",{"EN":213},"Short-term intensive fasting enhances the immune function of red blood cells in humans",{"VOID":215},"[\"10168944274606413420\"]",{"VOID":217},"Macario AJ, Conway de Macario E, Dugan CB. Erythroblasts can generate immunosuppression in vivo. Med (B Aires). 1981;41:83–90.\nElahi S. New insight into an old concept: role of immature erythroid cells in immune pathogenesis of neonatal infection. Front Immunol. 2014;5:376. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffimmu.2014.00376.\nElahi S, Ertelt JM, Kinder JM, Jiang TT, Zhang X, Xin L, et al. Immunosuppressive CD71 + erythroid cells compromise neonatal host defense against infection. Nature. 2013;504(7478):158–62. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fnature12675.\nDunsmore G, Bozorgmehr N, Delyea C, Koleva P, Namdar A, Elahi S. Erythroid suppressor cells compromise neonatal Immune response against Bordetella pertussis. J Immunol. 2017;199(6):2081–95. https:\u002F\u002Fdoi.org\u002F10.4049\u002Fjimmunol.1700742.\nShahbaz S, Bozorgmehr N, Koleva P, Namdar A, Jovel J, Fava RA, et al. CD71 + VISTA + erythroid cells promote the development and function of regulatory T cells through TGF-beta. PLoS Biol. 2018;16(12):e2006649. https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pbio.2006649.\nMiller D, Romero R, Unkel R, Xu Y, Vadillo-Ortega F, Hassan SS, et al. CD71 + erythroid cells from neonates born to women with preterm labor regulate cytokine and cellular responses. J Leukoc Biol. 2018;103(4):761–75. https:\u002F\u002Fdoi.org\u002F10.1002\u002FJLB.5A0717-291RRR.\nNelson RA. Jr. The immune-adherence phenomenon; an immunologically specific reaction between microorganisms and erythrocytes leading to enhanced phagocytosis. Science. 1953;118(3077):733–7. https:\u002F\u002Fdoi.org\u002F10.1126\u002Fscience.118.3077.733.\nCornacoff JB, Hebert LA, Smead WL, VanAman ME, Birmingham DJ, Waxman FJ. Primate erythrocyte-immune complex-clearing mechanism. J Clin Invest. 1983;71(2):236–47. https:\u002F\u002Fdoi.org\u002F10.1172\u002Fjci110764.\nHebert LA, Cosio G. The erythrocyte-immune complex-glomerulonephritis connection in man. Kidney Int. 1987;31(4):877–85. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fki.1987.81.\nEmlen W, Carl V, Burdick G. Mechanism of transfer of immune complexes from red blood cell CR1 to monocytes. Clin Exp Immunol. 1992;89(1):8–17. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fj.1365-2249.1992.tb06869.x.\nSchifferli JA, Ng YC, Estreicher J, Walport MJ. The clearance of tetanus toxoid\u002Fantitetanus toxoid immune complexes from the circulation of humans. Complement- and erythrocyte complement receptor 1-dependent mechanisms. J Immunol. 1988;140(3):899–904.\nDavies KA, Hird V, Stewart S, Sivolapenko GB, Jose P, Epenetos AA, et al. A study of in vivo immune complex formation and clearance in man. J Immunol. 1990;144(12):4613–20.\nKimberly RP, Edberg JC, Merriam LT, Clarkson SB, Unkeless JC, Taylor RP. In vivo handling of soluble complement fixing Ab\u002FdsDNA immune complexes in chimpanzees. J Clin Invest. 1989;84(3):962–70. https:\u002F\u002Fdoi.org\u002F10.1172\u002FJCI114259.\nMedof ME, Iida K, Mold C, Nussenzweig V. Unique role of the complement receptor CR1 in the degradation of C3b associated with immune complexes. J Exp Med. 1982;156(6):1739–54. https:\u002F\u002Fdoi.org\u002F10.1084\u002Fjem.156.6.1739.\nPascual M, Schifferli JA. Another function of erythrocytes: transport of circulating immune complexes. Infusionsther Transfusionsmed. 1995;22(5):310–5. https:\u002F\u002Fdoi.org\u002F10.1159\u002F000223148.\nXu C, He J, Wang H, Zhang Y, Wu J, Zhao L, et al. Single-cell transcriptomic analysis identifies an immune-prone population in erythroid precursors during human ontogenesis. Nat Immunol. 2022;23(7):1109–20. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41590-022-01245-8.\nCollins N, Han SJ, Enamorado M, Link VM, Huang B, Moseman EA, et al. The bone marrow protects and optimizes immunological memory during Dietary Restriction. Cell. 2019;178(5):1088–101e15. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cell.2019.07.049.\nNagai M, Noguchi R, Takahashi D, Morikawa T, Koshida K, Komiyama S, et al. Fasting-refeeding impacts Immune Cell Dynamics and Mucosal Immune responses. Cell. 2019;178(5):1072–87e14. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cell.2019.07.047.\nJordan S, Tung N, Casanova-Acebes M, Chang C, Cantoni C, Zhang D, et al. Dietary intake regulates the circulating inflammatory Monocyte Pool. Cell. 2019;178(5):1102–14e17. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cell.2019.07.050.\nJanssen H, Kahles F, Liu D, Downey J, Koekkoek LL, Roudko V, et al. Monocytes re-enter the bone marrow during fasting and alter the host response to infection. Immunity. 2023. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.immuni.2023.01.024.\nQian J, Fang Y, Yuan N, Gao X, Lv Y, Zhao C, et al. Innate immune remodeling by short-term intensive fasting. Aging Cell. 2021;20(11):e13507. https:\u002F\u002Fdoi.org\u002F10.1111\u002Facel.13507.\nWu T, Hu E, Xu S, Chen M, Guo P, Dai Z, et al. clusterProfiler 4.0: a universal enrichment tool for interpreting omics data. Innov (Camb). 2021;2(3):100141. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.xinn.2021.100141.\nPaccaud JP, Carpentier JL, Schifferli JA. Direct evidence for the clustered nature of complement receptors type 1 on the erythrocyte membrane. J Immunol. 1988;141(11):3889–94.\nPapadopoulos C, Spourita E, Tentes I, Steiropoulos P, Anagnostopoulos K. Red Blood Cell Malfunction in COVID-19: Molecular Mechanisms and therapeutic targets. Viral Immunol. 2022;35(10):649–52. https:\u002F\u002Fdoi.org\u002F10.1089\u002Fvim.2021.0212.\nLam LM, Murphy SJ, Reilly JP, Rux AH, Murphy SJ, Kuri-Cervantes L, et al. Erythrocytes identify complement activation in patients with COVID-19. Am J Physiol Lung Cell Mol Physiol. 2021. https:\u002F\u002Fdoi.org\u002F10.1152\u002Fajplung.00231.2021.\nKisserli A, Schneider N, Audonnet S, Tabary T, Goury A, Cousson J, et al. Acquired decrease of the C3b\u002FC4b receptor (CR1, CD35) and increased C4d deposits on erythrocytes from ICU COVID-19 patients. Immunobiology. 2021;226(3):152093. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.imbio.2021.152093.\nDamiani E, Adrario E, Luchetti MM, Scorcella C, Carsetti A, Mininno N, et al. Plasma free hemoglobin and microcirculatory response to fresh or old blood transfusions in sepsis. PLoS ONE. 2015;10(5):e0122655. https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0122655.\nMacDonald R. Red cell 2,3-diphosphoglycerate and oxygen affinity. Anesthesia. 1977;32(6):544–53. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fj.1365-2044.1977.tb10002.x.\nNauta AJ, Daha MR, Tijsma O, van de Water B, Tedesco F, Roos A. The membrane attack complex of complement induces caspase activation and apoptosis. Eur J Immunol. 2002;32(3):783–92. https:\u002F\u002Fdoi.org\u002F10.1002\u002F1521-4141(200203)32:3\u003C783::AID-IMMU783>3.0.CO;2-Q.\nDobkin J, Mangalmurti NS. Immunomodulatory roles of red blood cells. Curr Opin Hematol. 2022;29(6):306–9. https:\u002F\u002Fdoi.org\u002F10.1097\u002FMOH.0000000000000734.\nSennikov SV, Injelevskaya TV, Krysov SV, Silkov AN, Kovinev IB, Dyachkova NJ, et al. Production of hemo- and immunoregulatory cytokines by erythroblast antigen + and glycophorin A + cells from human bone marrow. BMC Cell Biol. 2004;5(1):39. https:\u002F\u002Fdoi.org\u002F10.1186\u002F1471-2121-5-39.\nKarsten E, Herbert BR. The emerging role of red blood cells in cytokine signaling and modulating immune cells. Blood Rev. 2020;41:100644. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.blre.2019.100644.\nFang Y, Gu Y, Zhao C, Lv Y, Qian J, Zhu L, et al. Impact of supervised beego, a traditional chinese water-only fasting, on thrombosis and hemostasis. BMJ Nutr Prev Health. 2021;4(1):4–17. https:\u002F\u002Fdoi.org\u002F10.1136\u002Fbmjnph-2020-000183.\nBarradas M, Plaza A, Colmenarejo G, Lazaro I, Costa-Machado LF, Martin-Hernandez R, et al. Fatty acids homeostasis during fasting predicts protection from chemotherapy toxicity. Nat Commun. 2022;13(1):5677. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41467-022-33352-3.\nCarvelli J, Demaria O, Vely F, Batista L, Chouaki Benmansour N, Fares J, et al. Association of COVID-19 inflammation with activation of the C5a-C5aR1 axis. Nature. 2020;588(7836):146–50. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41586-020-2600-6.\nHolter JC, Pischke SE, de Boer E, Lind A, Jenum S, Holten AR, et al. Systemic complement activation is associated with respiratory failure in COVID-19 hospitalized patients. Proc Natl Acad Sci U S A. 2020;117(40):25018–25. https:\u002F\u002Fdoi.org\u002F10.1073\u002Fpnas.2010540117.\nRisitano AM, Mastellos DC, Huber-Lang M, Yancopoulou D, Garlanda C, Ciceri F, et al. Complement as a target in COVID-19? 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aging leads to immune dysfunction, significantly reducing the quality of life of the elderly. Aged-related defects in early hematopoiesis result in reduced lymphoid cell development, functionally defective mature immune cells, and poor protective responses to vaccines and pathogens. Despite considerable progress understanding the underlying causes of decreased immunity in the elderly, the mechanisms by which these occur are still poorly understood. The DNA-binding protein ARID3a is expressed in a subset of human hematopoietic progenitors. Inhibition of ARID3a in bulk human cord blood CD34+ hematopoietic progenitors led to developmental skewing toward myeloid lineage at the expense of lymphoid lineage cells in vitro. Effects of ARID3a expression in adult-derived hematopoietic stem cells (HSCs) have not been analyzed, nor has ARID3a expression been assessed in relationship to age. We hypothesized that decreases in ARID3a could explain some of the defects observed in aging. Our data reveal decreased frequencies of ARID3a-expressing peripheral blood HSCs from aged healthy individuals compared with young donor HSCs. Inhibition of ARID3a in young donor-derived HSCs limits B lineage potential, suggesting a role for ARID3a in B lymphopoiesis in bone marrow-derived HSCs. Increasing ARID3a levels of HSCs from aged donors in vitro alters B lineage development and maturation. Finally, single cell analyses of ARID3a-expressing HSCs from young versus aged donors identify a number of differentially expressed genes in aged ARID3A-expressing cells versus young ARID3A-expressing HSCs, as well as between ARID3A-expressing and non-expressing cells in both young and aged donor HSCs. These data suggest that ARID3a-expressing HSCs from aged individuals differ at both molecular and functional levels compared to ARID3a-expressing HSCs from young individuals.",{"EN":714},"ARID3a expression in human hematopoietic stem cells is associated with distinct gene patterns in aged individuals",{"VOID":716},"[\"2100468721824261138\"]",{"VOID":718},"Colby SL, Ortman JM. Projections of the Size and Composition of the U.S. Population: 2014 to 2060. Population Estimates and Projections. Current Population Reports. P25–1143. Numerical\u002FQuantitative Data Report. Washington, DC: US Census Bureau; 2015. Tel: 800–923-8282; Tel: 301–763-4636; e-mail: Census.in.Schools@census.gov; Web site: http:\u002F\u002Fwww.census.gov\u002F; Report No.: ED578934.\nPang WW, Schrier SL, Weissman IL. Age-associated changes in human hematopoietic stem cells. Semin Hematol. 2017;54(1):39–42.\nLaurenti E, Gottgens B. From haematopoietic stem cells to complex differentiation landscapes. Nature. 2018;553(7689):418–26.\nDykstra B, Olthof S, Schreuder J, Ritsema M, de Haan G. Clonal analysis reveals multiple functional defects of aged murine hematopoietic stem cells. J Exp Med. 2011;208(13):2691–703.\nKuranda K, Vargaftig J, de la Rochere P, Dosquet C, Charron D, Bardin F, et al. Age-related changes in human hematopoietic stem\u002Fprogenitor cells. Aging Cell. 2011;10(3):542–6.\nPang WW, Price EA, Sahoo D, Beerman I, Maloney WJ, Rossi DJ, et al. Human bone marrow hematopoietic stem cells are increased in frequency and myeloid-biased with age. Proc Natl Acad Sci U S A. 2011;108(50):20012–7.\nSun D, Luo M, Jeong M, Rodriguez B, Xia Z, Hannah R, et al. Epigenomic profiling of young and aged HSCs reveals concerted changes during aging that reinforce self-renewal. Cell Stem Cell. 2014;14(5):673–88.\nFali T, Fabre-Mersseman V, Yamamoto T, Bayard C, Papagno L, Fastenackels S, et al. Elderly human hematopoietic progenitor cells express cellular senescence markers and are more susceptible to pyroptosis. JCI Insight. 2018;3(13):e95319.\nFlach J, Bakker ST, Mohrin M, Conroy PC, Pietras EM, Reynaud D, et al. Replication stress is a potent driver of functional decline in ageing haematopoietic stem cells. Nature. 2014;512(7513):198–202.\nKortschak RD, Tucker PW, Saint R. ARID proteins come in from the desert. Trends Biochem Sci. 2000;25(6):294–9.\nPatsialou A, Wilsker D, Moran E. DNA-binding properties of ARID family proteins. Nucleic Acids Res. 2005;33(1):66–80.\nRatliff ML, Templeton TD, Ward JM, Webb CF. The bright side of hematopoiesis: regulatory roles of ARID3a\u002Fbright in human and mouse hematopoiesis. Front Immunol. 2014;5:113.\nPopowski M, Templeton TD, Lee BK, Rhee C, Li H, Miner C, et al. Bright\u002FArid3A acts as a barrier to somatic cell reprogramming through direct regulation of Oct4, Sox2, and Nanog. Stem Cell Rep. 2014;2(1):26–35.\nRajaiya J, Nixon JC, Ayers N, Desgranges ZP, Roy AL, Webb CF. Induction of immunoglobulin heavy-chain transcription through the transcription factor bright requires TFII-I. Mol Cell Biol. 2006;26(12):4758–68.\nRajaiya J, Hatfield M, Nixon JC, Rawlings DJ, Webb CF. Bruton’s tyrosine kinase regulates immunoglobulin promoter activation in association with the transcription factor bright. Mol Cell Biol. 2005;25(6):2073–84.\nLin D, Ippolito GC, Zong RT, Bryant J, Koslovsky J, Tucker P. Bright\u002FARID3A contributes to chromatin accessibility of the immunoglobulin heavy chain enhancer. Mol Cancer. 2007;6:23.\nWard JM, Ratliff ML, Dozmorov MG, Wiley G, Guthridge JM, Gaffney PM, et al. Expression and methylation data from SLE patient and healthy control blood samples subdivided with respect to ARID3a levels. Data Brief. 2016;9:213–9.\nWard JM, Ratliff ML, Dozmorov MG, Wiley G, Guthridge JM, Gaffney PM, et al. Human effector B lymphocytes express ARID3a and secrete interferon alpha. J Autoimmun. 2016;75:130–40.\nWebb CF, Bryant J, Popowski M, Allred L, Kim D, Harriss J, et al. The ARID family transcription factor bright is required for both hematopoietic stem cell and B lineage development. Mol Cell Biol. 2011;31(5):1041–53.\nNixon JC, Ferrell S, Miner C, Oldham AL, Hochgeschwender U, Webb CF. Transgenic mice expressing dominant-negative bright exhibit defects in B1 B cells. J Immunol. 2008;181(10):6913–22.\nHayakawa K, Li YS, Shinton SA, Bandi SR, Formica AM, Brill-Dashoff J, et al. Crucial role of increased Arid3a at the pre-B and immature B cell stages for B1a cell generation. Front Immunol. 2019;10:457.\nLi YS, Zhou Y, Tang L, Shinton SA, Hayakawa K, Hardy RR. A developmental switch between fetal and adult B lymphopoiesis. Ann N Y Acad Sci. 2015;1362:8–15.\nZhou Y, Li YS, Bandi SR, Tang L, Shinton SA, Hayakawa K, et al. Lin28b promotes fetal B lymphopoiesis through the transcription factor Arid3a. J Exp Med. 2015;212(4):569–80.\nSimell B, Vuorela A, Ekstrom N, Palmu A, Reunanen A, Meri S, et al. Aging reduces the functionality of anti-pneumococcal antibodies and the killing of Streptococcus pneumoniae by neutrophil phagocytosis. Vaccine. 2011;29(10):1929–34.\nBrooks LRK, Mias GI. Streptococcus pneumoniae’s virulence and host immunity: aging, diagnostics, and prevention. Front Immunol. 2018;9:1366.\nOldham AL, Miner CA, Wang HC, Webb CF. The transcription factor bright plays a role in marginal zone B lymphocyte development and autoantibody production. Mol Immunol. 2011;49(1–2):367–79.\nBaumgarth N. A hard(y) look at B-1 cell development and function. J Immunol. 2017;199(10):3387–94.\nSanz I, Wei C, Jenks SA, Cashman KS, Tipton C, Woodruff MC, et al. Challenges and opportunities for consistent classification of human B cell and plasma cell populations. Front Immunol. 2019;10:2458.\nRatliff ML, Ward JM, Merrill JT, James JA, Webb CF. Differential expression of the transcription factor ARID3a in lupus patient hematopoietic progenitor cells. J Immunol. 2015;194(3):940–9.\nRatliff ML, Mishra M, Frank MB, Guthridge JM, Webb CF. The transcription factor ARID3a is important for in vitro differentiation of human hematopoietic progenitors. J Immunol. 2016;196(2):614–23.\nRossi DJ, Bryder D, Zahn JM, Ahlenius H, Sonu R, Wagers AJ, et al. Cell intrinsic alterations underlie hematopoietic stem cell aging. Proc Natl Acad Sci U S A. 2005;102(26):9194–9.\nWahlestedt M, Norddahl GL, Sten G, Ugale A, Frisk MA, Mattsson R, et al. An epigenetic component of hematopoietic stem cell aging amenable to reprogramming into a young state. Blood. 2013;121(21):4257–64.\nZhang WG, Zhu SY, Bai XJ, Zhao DL, Jian SM, Li J, et al. Select aging biomarkers based on telomere length and chronological age to build a biological age equation. Age (Dordr). 2014;36(3):9639.\nLee Y, Sun D, Ori APS, Lu AT, Seeboth A, Harris SE, et al. Epigenome-wide association study of leukocyte telomere length. Aging (Albany NY). 2019;11(16):5876–94.\nde Haan G, Lazare SS. Aging of hematopoietic stem cells. Blood. 2018;131(5):479–87.\nvan Galen P, Kreso A, Wienholds E, Laurenti E, Eppert K, Lechman ER, et al. Reduced lymphoid lineage priming promotes human hematopoietic stem cell expansion. Cell Stem Cell. 2014;14(1):94–106.\nCamous X, Pera A, Solana R, Larbi A. NK cells in healthy aging and age-associated diseases. J Biomed Biotechnol. 2012;2012:195956.\nCichocki F, Grzywacz B, Miller JS. Human NK cell development: one road or many? Front Immunol. 2019;10:2078.\nSanz E, Munoz AN, Monserrat J, Van-Den-Rym A, Escoll P, Ranz I, et al. Ordering human CD34+CD10-CD19+ pre\u002Fpro-B-cell and CD19- common lymphoid progenitor stages in two pro-B-cell development pathways. Proc Natl Acad Sci U S A. 2010;107(13):5925–30.\nDmytrus J, Matthes-Martin S, Pichler H, Worel N, Geyeregger R, Frank N, et al. Multi-color immune-phenotyping of CD34 subsets reveals unexpected differences between various stem cell sources. Bone Marrow Transplant. 2016;51(8):1093–100.\nMontecino-Rodriguez E, Dorshkind K. B-1 B cell development in the fetus and adult. Immunity. 2012;36(1):13–21.\nDoulatov S, Notta F, Laurenti E, Dick JE. Hematopoiesis: a human perspective. Cell Stem Cell. 2012;10(2):120–36.\nPrzemska-Kosicka A, Childs CE, Maidens C, Dong H, Todd S, Gosney MA, et al. Age-related changes in the natural killer cell response to seasonal influenza vaccination are not influenced by a Synbiotic: a randomised controlled trial. Front Immunol. 2018;9:591.\nIchii M, Oritani K, Yokota T, Schultz DC, Holter JL, Kanakura Y, et al. Stromal cell-free conditions favorable for human B lymphopoiesis in culture. 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Ann N Y Acad Sci. 2015;1362(1):176–87.\nCancro MP. Age-associated B Cells. Annu Rev Immunol. 2020;38:315–40.\nHao Y, O'Neill P, Naradikian MS, Scholz JL, Cancro MP. A B-cell subset uniquely responsive to innate stimuli accumulates in aged mice. Blood. 2011;118(5):1294–304.\nRubtsov AV, Rubtsova K, Fischer A, Meehan RT, Gillis JZ, Kappler JW, et al. Toll-like receptor 7 (TLR7)-driven accumulation of a novel CD11c(+) B-cell population is important for the development of autoimmunity. Blood. 2011;118(5):1305–15.\nRundberg Nilsson A, Soneji S, Adolfsson S, Bryder D, Pronk CJ. Human and murine hematopoietic stem cell aging is associated with functional impairments and intrinsic megakaryocytic\u002FErythroid bias. PLoS One. 2016;11(7):e0158369.\nNotta F, Doulatov S, Laurenti E, Poeppl A, Jurisica I, Dick JE. Isolation of single human hematopoietic stem cells capable of long-term multilineage engraftment. Science (New York, NY). 2011;333(6039):218–21.\nNixon JC, Rajaiya JB, Ayers N, Evetts S, Webb CF. The transcription factor, bright, is not expressed in all human B lymphocyte subpopulations. Cell Immunol. 2004;228(1):42–53.\nTomellini E, Fares I, Lehnertz B, Chagraoui J, Mayotte N, MacRae T, et al. Integrin-alpha3 Is a Functional Marker of Ex Vivo Expanded Human Long-Term Hematopoietic Stem Cells. Cell Rep. 2019;28(4):1063–73.e5.",{"VOID":720},"10.1186\u002Fs12979-020-00198-6","2024-06-26T22:37:08.286+00:00","https:\u002F\u002Fimmunityageing.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12979-020-00198-6",[724,769,796,821],{"id":725,"sortIndex":21,"researcher":20,"roles":726,"affiliations":727,"properties":764,"displayName":766,"givenName":20,"familyName":20},"b36002b4-ed13-4512-a4f1-a38934f009d2",[127],[728,738,746,754],{"id":729,"sortIndex":21,"affiliation":730,"properties":736},"a8ce8f35-5f65-4c98-a1b6-d48bb0d7de0b",{"id":729,"createTime":20,"updateTime":20,"relativeEntities":731,"slug":20,"properties":732,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":735,"statistic":20},[],{"title":733},{"VI":734},"Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, USA",[],{"title":737},{"VI":734},{"id":739,"sortIndex":21,"affiliation":740,"properties":20},"8c0b185e-62e3-4d5c-b24f-5b21a627e9d3",{"id":739,"createTime":20,"updateTime":20,"relativeEntities":741,"slug":20,"properties":742,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":745,"statistic":20},[],{"title":743},{"VI":744},"Arthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, USA",[],{"id":747,"sortIndex":21,"affiliation":748,"properties":20},"14f1e86c-b239-4b90-a43f-57da10f7c53d",{"id":747,"createTime":20,"updateTime":20,"relativeEntities":749,"slug":20,"properties":750,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":753,"statistic":20},[],{"title":751},{"VI":752},"Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, USA",[],{"id":755,"sortIndex":21,"affiliation":756,"properties":762},"294d8c43-eb7a-4841-845c-b057281c79e3",{"id":755,"createTime":20,"updateTime":20,"relativeEntities":757,"slug":20,"properties":758,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":761,"statistic":20},[],{"title":759},{"VI":760},"Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, USA",[],{"title":763},{"VI":760},{"title":765,"gsAuthor":767},{"VI":766},"Judith A. 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Inhibition of autophagic capacity with ageing was postulated to generate a pro-inflammatory condition via activation of inflammasomes, a group of Interleukin-1 activating intracellular multi-protein complexes. We thus investigated gene expression of inflammasome components in PBMC of 77 vascular patients (age 22–82) in association with age. Linear regression of real-time qRT-PCR data revealed a significant positive association of gene expression of each of the inflammasome components with age (Pearson correlation coefficients: AIM2: r = 0.245; P = 0.032; NLRP3: r = 0.367; P = 0.001; ASC (PYCARD): r = 0.252; P = 0.027; CASP1: r = 0.296; P = 0.009; CASP5: r = 0.453; P = 0.00003; IL1B: r = 0.247; P = 0.030). No difference in gene expression of AIM2, NLRP3, ASC CASP1, and CASP5 was detected between PBMC of patients with advanced atherosclerosis and other vascular patients, whereas IL1B expression was increased in PBMC of the latter group (P = 0.0005). The findings reinforce the systemic pro-inflammatory phenotype reported in elderly by demonstrating an increased phase-1 activation of inflammasomes in PBMC of vascular patients.",{"EN":906},"Gene expression of inflammasome components in peripheral blood mononuclear cells (PBMC) of vascular patients increases with age",{"VOID":908},"[\"2533081225529867316\"]",{"VOID":910},"Franceschi C, Bonafè M, Valensin S, Olivieri F, De Luca M, Ottaviani E, et al. Inflamm-aging. An evolutionary perspective on immunosenescence. Ann N Y Acad Sci. 2000;908:244–54.\nLarbi A, Franceschi C, Mazzatti D, Solana R, Wikby A, Pawelec G. Aging of the immune system as a prognostic factor for human longevity. Physiology (Bethesda). 2008;23:64–74.\nKovacs EJ, Palmer JL, Fortin CF, Fülöp Jr T, Goldstein DR, Linton PJ. Aging and innate immunity in the mouse: impact of intrinsic and extrinsic factors. Trends Immunol. 2009;30(7):319–24.\nPinke KH, Calzavara B, Faria PF, do Nascimento MP, Venturini J, Lara VS. Proinflammatory profile of in vitro monocytes in the ageing is affected by lymphocytes presence. Immun Ageing. 2013;10(1):22.\nFerrucci L, Corsi A, Lauretani F, Bandinelli S, Bartali B, Taub DD, et al. The origins of age-related proinflammatory state. Blood. 2005;105(6):2294–9.\nDinarello CA. Interleukin-1beta and the autoinflammatory diseases. N Engl J Med. 2009;360(23):2467–70.\nFeldman, N., A. Rotter-Maskowitz, and E. Okun, DAMPs as mediators of sterile inflammation in aging-related pathologies. Ageing Res Rev, 2015. doi: 10.1016\u002Fj.arr.2015.01.003.\nGoldberg R, Prescott N, Lord GM, MacDonald TT, Powell N. The unusual suspects-innate lymphoid cells as novel therapeutic targets in IBD. Nat Rev Gastroenterol Hepatol. 2015;12(5):271–83.\nSalminen A, Kaarniranta K, Kauppinen A. Inflammaging: disturbed interplay between autophagy and inflammasomes. Aging (Albany NY). 2012;4(3):166–75.\nLatz E, Xiao TS, Stutz A. Activation and regulation of the inflammasomes. Nat Rev Immunol. 2013;13(6):397–411.\nKono H, Kimura Y, Latz E. Inflammasome activation in response to dead cells and their metabolites. Curr Opin Immunol. 2014;30:91–8.\nDuewell P, Kono H, Rayner KJ, Sirois CM, Vladimer G, Bauernfeind FG, et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature. 2010;464(7293):1357–61.\nDihlmann S, Erhart P, Mehrabi A, Nickkholgh A, Lasitschka F, Böckler D, et al. Increased expression and activation of absent in melanoma 2 inflammasome components in lymphocytic infiltrates of abdominal aortic aneurysms. Mol Med. 2014;20(1):230–7.\nHakimi M, Peters A, Becker A, Böckler D, Dihlmann S. Inflammation-related induction of absent in melanoma 2 (AIM2) in vascular cells and atherosclerotic lesions suggests a role in vascular pathogenesis. J Vasc Surg. 2014;59(3):794–803. e2.\nSamstad EO, Niyonzima N, Nymo S, Aune MH, Ryan L, Bakke SS, et al. Cholesterol crystals induce complement-dependent inflammasome activation and cytokine release. J Immunol. 2014;192(6):2837–45.\nGolledge AL, Walker P, Norman PE, Golledge J. A systematic review of studies examining inflammation associated cytokines in human abdominal aortic aneurysm samples. Dis Markers. 2009;26(4):181–8.\nYoum YH, Grant RW, McCabe LR, Albarado DC, Nguyen KY, Ravussin A, et al. Canonical Nlrp3 inflammasome links systemic low-grade inflammation to functional decline in aging. Cell Metab. 2013;18(4):519–32.\nSpencer NF, Poynter ME, Im SY, Daynes RA. Constitutive activation of NF-kappa B in an animal model of aging. Int Immunol. 1997;9(10):1581–8.\nXiao ZQ, Majumdar AP. Induction of transcriptional activity of AP-1 and NF-kappaB in the gastric mucosa during aging. Am J Physiol Gastrointest Liver Physiol. 2000;278(6):G855–65.\nHelenius M, Kyrylenko S, Vehviläinen P, Salminen A. Characterization of aging-associated up-regulation of constitutive nuclear factor-kappa B binding activity. Antioxid Redox Signal. 2001;3(1):147–56.\nDuan X, Ponomareva L, Veeranki S, Panchanathan R, Dickerson E, Choubey D. Differential Roles for the Interferon-Inducible IFI16 and AIM2 Innate Immune Sensors for Cytosolic DNA in Cellular Senescence of Human Fibroblasts. Mol Cancer Res. 2011;9(5):589–602.\nDella Bella S, Bierti L, Presicce P, Arienti R, Valenti M, Saresella M, et al. Peripheral blood dendritic cells and monocytes are differently regulated in the elderly. Clin Immunol. 2007;122(2):220–8.\nLorton D, Bellinger DL. Molecular mechanisms underlying beta-adrenergic receptor-mediated cross-talk between sympathetic neurons and immune cells. Int J Mol Sci. 2015;16(3):5635–65.\nSantulli G, Iaccarino G. Pinpointing beta adrenergic receptor in ageing pathophysiology: victim or executioner? Evidence from crime scenes. Immun Ageing. 2013;10(1):10.",{"VOID":912},"10.1186\u002Fs12979-015-0043-y","2024-05-16T13:38:33.689+00:00","http:\u002F\u002Fwww.immunityageing.com\u002Fcontent\u002F12\u002F1\u002F15",[916,940,962,975,988,1001],{"id":917,"sortIndex":21,"researcher":20,"roles":918,"affiliations":919,"properties":937,"displayName":939,"givenName":20,"familyName":20},"2d3d45f0-2a4f-4fb0-b0d0-39d9205a748b",[127],[920,928],{"id":921,"sortIndex":21,"affiliation":922,"properties":20},"92ae8409-82a0-4cc8-870c-52d5f2497df0",{"id":921,"createTime":20,"updateTime":20,"relativeEntities":923,"slug":20,"properties":924,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":927,"statistic":20},[],{"title":925},{"VI":926},"Department of Vascular and Endovascular Surgery, University of Heidelberg, Heidelberg, 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               \u003Cjats:title>Background\u003C\u002Fjats:title>\n                \u003Cjats:p>Obesity is associated with chronic low-grade inflammation leading to metabolic and cardiovascular diseases, but a subset of obese individuals is considered insulin sensitive (IS). The underlying pathophysiologic mechanisms remain elusive and clinical studies on the relationship between inflammatory markers and metabolically healthy obesity (MHO) are scarce.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Methods\u003C\u002Fjats:title>\n                \u003Cjats:p>In this cross-sectional analysis, we included a sample of 437 older participants (60–84 years) from the Berlin Aging Study II (BASE-II). Peripheral blood mononuclear cells were isolated, immune cell subsets were analyzed with multiparameter flow cytometry and systemic cytokine levels were measured. Immune cell parameters were correlated with metabolic measures and multiple linear regression analysis was conducted and adjusted for various demographic and clinical factors.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Results\u003C\u002Fjats:title>\n                \u003Cjats:p>We found that frequencies of naïve and memory CD4\u003Cjats:sup>+\u003C\u002Fjats:sup> and CD8\u003Cjats:sup>+\u003C\u002Fjats:sup> T cells inversely correlated with measures for insulin sensitivity in the older population. Moreover, the percentages of naïve CD4\u003Cjats:sup>+\u003C\u002Fjats:sup> and CD8\u003Cjats:sup>+\u003C\u002Fjats:sup> T cells were significantly higher, whereas activated T cells and IL-6 levels were lower in IS compared to insulin resistant (IR) obese individuals. The percentages of naïve CD4\u003Cjats:sup>+\u003C\u002Fjats:sup> and CD8\u003Cjats:sup>+\u003C\u002Fjats:sup> T cells were predictive for impaired insulin sensitivity (ß = 0.16, \u003Cjats:italic>p\u003C\u002Fjats:italic> = 0.01 and ß = 0.11, \u003Cjats:italic>p\u003C\u002Fjats:italic> = 0.04), and the association of naïve CD4\u003Cjats:sup>+\u003C\u002Fjats:sup> T cells with insulin sensitivity persisted after multivariate adjustment (ß = 0.14, \u003Cjats:italic>p\u003C\u002Fjats:italic> = 0.02).\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Conclusions\u003C\u002Fjats:title>\n                \u003Cjats:p>These findings support the hypothesis that parameters of systemic inflammation can differentiate IS from IR obese individuals that are at higher risk for cardiometabolic diseases and may have clinical implications with regard to obesity treatment stratification.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Trial registration\u003C\u002Fjats:title>\n                \u003Cjats:p>\u003Cjats:ext-link xmlns:xlink=\"http:\u002F\u002Fwww.w3.org\u002F1999\u002Fxlink\" ext-link-type=\"uri\" xlink:href=\"https:\u002F\u002Fwww.base2.mpg.de\u002Fen\">DRKS00009277\u003C\u002Fjats:ext-link>. Registered 31 August 2015 - Retrospectively registered.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>",{"EN":1086},"T cell phenotypes associated with insulin resistance: results from the Berlin Aging Study 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Immun Ageing. 2020;17(1):15.",{"doi":1409},"10.1186\u002Fs12979-020-00186-w",{"id":20,"text":1411,"url":20,"identifiers":1412},"Di Benedetto S, Derhovanessian E, Steinhagen-Thiessen E, Goldeck D, Müller L, Pawelec G. Impact of age, sex and CMV-infection on peripheral T cell phenotypes: results from the Berlin BASE-II study. Biogerontology. 2015;16(5):631–43.",{"doi":1413},"10.1007\u002Fs10522-015-9563-2",{"id":20,"text":1415,"url":20,"identifiers":1416},"Tam BT, Morais JA, Santosa S. Obesity and ageing: two sides of the same coin. Obes Rev. 2020;21(4):e12991.",{"doi":1417},"10.1111\u002Fobr.12991",{"id":20,"text":1419,"url":20,"identifiers":1420},"Fulop T, Witkowski JM, Pawelec G, Alan C, Larbi A. On the immunological theory of aging. Interdiscip Top Gerontol. 2014;39:163-76. https:\u002F\u002Fdoi.org\u002F10.1159\u002F000358904.",{"doi":1421},"10.1159\u002F000358904",{"id":20,"text":1423,"url":20,"identifiers":1424},"Kverneland AH, Streitz M, Geissler E, Hutchinson J, Vogt K, Boës D, et al. Age and gender leucocytes variances and references values generated using the standardized ONE-study protocol. Cytometry Part A. 2016;89(6):543–64.",{"doi":1425},"10.1002\u002Fcyto.a.22855",{"id":20,"text":1427,"url":20,"identifiers":1428},"Streitz M, Miloud T, Kapinsky M, Reed MR, Magari R, Geissler EK, et al. Standardization of whole blood immune phenotype monitoring for clinical trials: panels and methods from the ONE study. Transplant Res. 2013;2:17.",{"doi":1429},"10.1186\u002F2047-1440-2-17",{"id":20,"text":1431,"url":20,"identifiers":1432},"Müller L, Fülöp T, Pawelec G. Immunosenescence in vertebrates and invertebrates. Immun Ageing. 2013;10(1):12.",{"doi":1433},"10.1186\u002F1742-4933-10-12",{"id":20,"text":1435,"url":20,"identifiers":1436},"Tegeler C, O'Sullivan JL, Bucholtz N, Goldeck D, Pawelec G, Steinhagen-Thiessen E, et al. The inflammatory markers CRP, IL-6, and IL-10 are associated with cognitive function—data from the Berlin aging study II. Neurobiol Aging. 2016;38:112–7.",{"doi":1437},"10.1016\u002Fj.neurobiolaging.2015.10.039",{"id":20,"text":1439,"url":20,"identifiers":1440},"McNelis JC, Olefsky JM. Macrophages, immunity, and metabolic disease. Immunity. 2014;41(1):36-48. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.immuni.2014.05.010.",{"doi":1441},"10.1016\u002Fj.immuni.2014.05.010",{"id":20,"text":1443,"url":20,"identifiers":1444},"Ferrante AW. Macrophages, fat, and the emergence of immunometabolism. J Clin Invest. 2013;123(12):4992–3.",{"doi":1445},"10.1172\u002FJCI73658",{"id":20,"text":1447,"url":20,"identifiers":1448},"Liu J, Divoux A, Sun J, Zhang J, Clément K, Glickman JN, et al. Genetic deficiency and pharmacological stabilization of mast cells reduce diet-induced obesity and diabetes in mice. Nat Med. 2009;15:940.",{"doi":1449},"10.1038\u002Fnm.1994",{"id":20,"text":1451,"url":20,"identifiers":1452},"Talukdar S, Oh DY, Bandyopadhyay G, Li D, Xu J, McNelis J, et al. Neutrophils mediate insulin resistance in high fat diet fed mice via secreted elastase. Nat Med. 2012;18(9):1407–12.",{"doi":1453},"10.1038\u002Fnm.2885",{"id":20,"text":1455,"url":20,"identifiers":1456},"Stefanovic-Racic M, Yang X, Turner MS, Mantell BS, Stolz DB, Sumpter TL, et al. Dendritic cells promote macrophage infiltration and comprise a substantial proportion of obesity-associated increases in CD11c\u003Csup>+\u003C\u002Fsup> cells in adipose tissue and liver. Diabetes. 2012;61(9):2330–9.",{"doi":1457},"10.2337\u002Fdb11-1523",{"id":20,"text":1459,"url":20,"identifiers":1460},"Nishimura S, Manabe I, Nagasaki M, Eto K, Yamashita H, Ohsugi M, et al. CD8+ effector T cells contribute to macrophage recruitment and adipose tissue inflammation in obesity. Nat Med. 2009;15(8):914–20.",{"doi":1461},"10.1038\u002Fnm.1964",{"id":20,"text":1463,"url":20,"identifiers":1464},"Winer DA, Winer S, Shen L, Wadia PP, Yantha J, Paltser G, et al. B cells promote insulin resistance through modulation of T cells and production of pathogenic IgG antibodies. Nat Med. 2011;17:610.",{"doi":1465},"10.1038\u002Fnm.2353",{"id":20,"text":1467,"url":20,"identifiers":1468},"Onodera T, Fukuhara A, Jang MH, Shin J, Aoi K, Kikuta J, Otsuki M, Ishii M, Shimomura I. Adipose tissue macrophages induce PPARγ-high FOXP3(+) regulatory T cells. Sci Rep. 2015;5:16801. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fsrep16801.",{"doi":1469},"10.1038\u002Fsrep16801",{"id":20,"text":1471,"url":20,"identifiers":1472},"Zhao R, Tang D, Yi S, Li W, Wu C, Lu Y, et al. Elevated peripheral frequencies of Th22 cells: a novel potent participant in obesity and type 2 diabetes. Plos One. 2014;9(1):e85770.",{"doi":1473},"10.1371\u002Fjournal.pone.0085770",{"id":20,"text":1475,"url":20,"identifiers":1476},"Wagner N-M, Brandhorst G, Czepluch F, Lankeit M, Eberle C, Herzberg S, et al. Circulating regulatory T cells are reduced in obesity and may identify subjects at increased metabolic and cardiovascular risk. Obesity. 2013;21(3):461–8.",{"doi":1477},"10.1002\u002Foby.20087",{"id":20,"text":1479,"url":20,"identifiers":1480},"Wu H, Ghosh S, Perrard XD, Feng L, Garcia GE, Perrard JL, et al. T-cell accumulation and regulated on activation, Normal T cell expressed and secreted Upregulation in adipose tissue in obesity. Circulation. 2007;115(8):1029–38.",{"doi":1481},"10.1161\u002FCIRCULATIONAHA.106.638379",{"id":20,"text":1483,"url":20,"identifiers":1484},"Wu D, Han JM, Yu X, Lam AJ, Hoeppli RE, Pesenacker AM, et al. Characterization of regulatory T cells in obese omental adipose tissue in humans. Eur J Immunol. 2019;49(2):336–47.",{"doi":1485},"10.1002\u002Feji.201847570",{"id":20,"text":1487,"url":20,"identifiers":1488},"Bähr I, Jahn J, Zipprich A, Pahlow I, Spielmann J, Kielstein H. Impaired natural killer cell subset phenotypes in human obesity. Immunol Res. 2018;66(2):234–44.",{"doi":1489},"10.1007\u002Fs12026-018-8989-4",{"id":20,"text":1491,"url":20,"identifiers":1492},"Fabbrini E, Cella M, McCartney SA, Fuchs A, Abumrad NA, Pietka TA, Chen Z, Finck BN, Han DH, Magkos F, Conte C, Bradley D, Fraterrigo G, Eagon JC, Patterson BW, Colonna M, Klein S. Association between specific adipose tissue CD4+ T-cell populations and insulin resistance in obese individuals. Gastroenterology. 2013;145(2):366–74.e1-3. https:\u002F\u002Fdoi.org\u002F10.1053\u002Fj.gastro.2013.04.010.",{"doi":1493},"10.1053\u002Fj.gastro.2013.04.010",{"id":20,"text":1495,"url":20,"identifiers":1496},"Carey AL, Steinberg GR, Macaulay SL, Thomas WG, Holmes AG, Ramm G, et al. Interleukin-6 increases insulin-stimulated glucose disposal in humans and glucose uptake and fatty acid oxidation in vitro via AMP-activated protein kinase. Diabetes. 2006;55(10):2688–97.",{"doi":1497},"10.2337\u002Fdb05-1404",{"id":20,"text":1499,"url":20,"identifiers":1500},"Koelman L, Pivovarova-Ramich O, Pfeiffer AFH, Grune T, Aleksandrova K. Cytokines for evaluation of chronic inflammatory status in ageing research: reliability and phenotypic characterisation. Immun Ageing. 2019;16(1):11.",{"doi":1501},"10.1186\u002Fs12979-019-0151-1",{"id":20,"text":1503,"url":20,"identifiers":1504},"Blüher M. Adipose tissue dysfunction contributes to obesity related metabolic diseases. Best Pract Res Clin Endocrinol Metab. 2013;27(2):163-77. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.beem.2013.02.005.",{"doi":1505},"10.1016\u002Fj.beem.2013.02.005",{"id":20,"text":1507,"url":20,"identifiers":1508},"Bertram L, Böckenhoff A, Demuth I, Düzel S, Eckardt R, Li S-C, et al. Cohort profile: the Berlin aging study II (BASE-II)†. Int J Epidemiol. 2013;43(3):703–12.",{"doi":1509},"10.1093\u002Fije\u002Fdyt018",{"id":20,"text":1511,"url":20,"identifiers":1512},"Gerstorf D, Bertram L, Lindenberger U, Pawelec G, Demuth I, Steinhagen-Thiessen E, Wagner G. G: Editorial. Gerontology. 2016;62:311-315. https:\u002F\u002Fdoi.org\u002F10.1159\u002F000441495.",{"doi":1513},"10.1159\u002F000441495",{"id":20,"text":1515,"url":20,"identifiers":1516},"Association of Thyroid Function with Handgrip Strength. Data from the study of health in Pomerania and the Berlin aging study II. Thyroid. 2019;29(9):1220–6.",{"doi":1517},"10.1089\u002Fthy.2018.0646",{"id":20,"text":1519,"url":20,"identifiers":1520},"König M, Drewelies J, Norman K, Spira D, Buchmann N, Hülür G, et al. Historical trends in modifiable indicators of cardiovascular health and self-rated health among older adults: Cohort differences over 20 years between the Berlin Aging Study (BASE) and the Berlin Aging Study II (BASE-II). Plos One. 2018;13(1):e0191699-e.",{"doi":1521},"10.1371\u002Fjournal.pone.0191699",{"id":20,"text":1523,"url":20,"identifiers":1524},"Matsuda M, DeFronzo RA. Insulin sensitivity indices obtained from oral glucose tolerance testing: comparison with the euglycemic insulin clamp. Diabetes Care. 1999;22(9):1462–70.",{"doi":1525},"10.2337\u002Fdiacare.22.9.1462",{"id":20,"text":1527,"url":20,"identifiers":1528},"Janssen N, Derhovanessian E, Demuth I, Arnaout F, Steinhagen-Thiessen E, Pawelec G. Responses of dendritic cells to TLR-4 stimulation are maintained in the elderly and resist the effects of CMV infection seen in the young. J Gerontol Series A. 2015;71(9):1117–23.",{"doi":1529},"10.1093\u002Fgerona\u002Fglv119",{"id":20,"text":1531,"url":20,"identifiers":1532},"Charlson ME, Pompei P, Ales KL, MacKenzie CR. A new method of classifying prognostic comorbidity in longitudinal studies: development and validation. J Chronic Dis. 1987;40(5):373–83.",{"doi":1533},"10.1016\u002F0021-9681(87)90171-8",{"id":20,"text":1535,"url":20,"identifiers":1536},"Meyer A, Salewsky B, Spira D, Steinhagen-Thiessen E, Norman K, Demuth I. Leukocyte telomere length is related to appendicular lean mass: cross-sectional data from the Berlin Aging Study II (BASE-II). Am J Clin Nutr. 2016;103(1):178–83. https:\u002F\u002Fdoi.org\u002F10.3945\u002Fajcn.115.116806.",{"doi":1537},"10.3945\u002Fajcn.115.116806",{"id":20,"text":1539,"url":20,"identifiers":1540},"Goldeck D, Oettinger L, Janssen N, Demuth I, Steinhagen-Thiessen E, Pawelec G. Cytomegalovirus infection minimally affects the frequencies of B-cell phenotypes in peripheral blood of younger and older adults. Gerontology. 2016;62(3):323–9.",{"doi":1541},"10.1159\u002F000382076",{"id":20,"text":1543,"url":20,"identifiers":1544},"Derhovanessian E, Maier AB, Beck R, Jahn G, Hähnel K, Slagboom PE, et al. Hallmark features of immunosenescence are absent in familial longevity. J Immunol. 2010;185(8):4618–24.",{"doi":1545},"10.4049\u002Fjimmunol.1001629",{"id":20,"text":1547,"url":20,"identifiers":1548},"Weide B, Martens A, Zelba H, Stutz C, Derhovanessian E, Di Giacomo AM, et al. Myeloid-derived suppressor cells predict survival of patients with advanced melanoma: comparison with regulatory T cells and NY-ESO-1- or melan-A-specific T cells. Clin Cancer Res. 2014;20(6):1601–9.",{"doi":1549},"10.1158\u002F1078-0432.CCR-13-2508",{"id":20,"text":1551,"url":20,"identifiers":1552},"Goldeck D, Pawelec G, Norman K, Steinhagen-Thiessen E, Oettinger L, Haehnel K, et al. No strong correlations between serum cytokine levels, CMV serostatus and hand-grip strength in older subjects in the Berlin BASE-II cohort. Biogerontology. 2016;17(1):189–98.",{"doi":1553},"10.1007\u002Fs10522-015-9577-9",{"id":1555,"createTime":1556,"updateTime":1557,"relativeEntities":1558,"slug":1559,"properties":1560,"entityType":118,"verifyStatus":119,"verifyTime":1573,"verifyNote":121,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1574,"fullTextUrl":20,"authors":1575,"publicationType":140,"publisherRelationship":1677,"citationCount":1723,"citationInfo":1724,"publishDate":1727,"publishYear":1725,"citationAnalyzeStatus":19,"lastCitationAnalyze":1728,"indexDatabases":1729,"openAccess":20,"references":20,"isForceReanalyzing":202},"da0d75e6-27e2-4e96-8006-f4ec926c6f29","2024-04-07T10:12:15.351+00:00","2026-01-27T07:19:32.733+00:00",[],"CpG-sites-associated-with-NRP1-NRXN2-and-miR-29b-2-are-hypomethylated-in-monocytes-during-ageing",{"abstract":1561,"title":1563,"gsPaper":1565,"keywords":1567,"references":1569,"doi":1571},{"EN":1562},"Ageing affects many components of the immune system, including innate immune cells like monocytes. They are important in the early response to pathogens and for their role to differentiate into macrophages and dendritic cells. Recent studies have revealed significant age-related changes in genomic DNA methylation in peripheral blood mononuclear cells, however information on epigenetic changes in specific leukocyte subsets is still lacking. Here, we aimed to analyse DNA methylation in purified monocyte populations from young and elderly individuals. We analysed the methylation changes in monocytes purified from young and elderly individuals using the HumanMethylation450 BeadChip array. Interestingly, we found that among 26 differentially methylated CpG sites, the majority of sites were hypomethylated in elderly individuals. The most hypomethylated CpG sites were located in neuropilin 1 (NRP1; cg24892069) and neurexin 2 (NRXN2; cg27209729) genes, and upstream of miR-29b-2 gene (cg10501210). The age-related hypomethylation of these three sites was confirmed in a separate group of young and elderly individuals. We identified significant age-related hypomethylation in human purified monocytes at CpG sites within the regions of NRP1, NRXN2 and miR-29b-2 genes.",{"EN":1564},"CpG sites associated with NRP1, NRXN2 and miR-29b-2 are hypomethylated in monocytes during ageing",{"VOID":1566},"[\"15924305618436835701\"]",{"EN":1568},"",{"VOID":1570},"Haynes L, Swain SL: Why aging T cells fail: implications for vaccination. Immunity. 2006, 24: 663-666. 10.1016\u002Fj.immuni.2006.06.003.\nKovaiou RD, Herndler-Brandstetter D, Grubeck-Loebenstein B: Age-related changes in immunity: implications for vaccination in the elderly. Expert Rev Mol Med. 2007, 9: 1-17.\nPanda A, Arjona A, Sapey E, Bai F, Fikrig E, Montgomery RR, Lord JM, Shaw AC: Human innate immunosenescence: causes and consequences for immunity in old age. Trends Immunol. 2009, 30: 325-333. 10.1016\u002Fj.it.2009.05.004.\nWeng NP: Aging of the immune system: how much can the adaptive immune system adapt?. Immunity. 2006, 24: 495-499. 10.1016\u002Fj.immuni.2006.05.001.\nShaw AC, Joshi S, Greenwood H, Panda A, Lord JM: Aging of the innate immune system. Curr Opin Immunol. 2010, 22: 507-513. 10.1016\u002Fj.coi.2010.05.003.\nNyugen J, Agrawal S, Gollapudi S, Gupta S: Impaired functions of peripheral blood monocyte subpopulations in aged humans. J Clin Immunol. 2010, 30: 806-813. 10.1007\u002Fs10875-010-9448-8.\nVasto S, Candore G, Balistreri CR, Caruso M, Colonna-Romano G, Grimaldi MP, Listi F, Nuzzo D, Lio D, Caruso C: Inflammatory networks in ageing, age-related diseases and longevity. Mech Ageing Dev. 2007, 128: 83-91. 10.1016\u002Fj.mad.2006.11.015.\nBell JT, Tsai PC, Yang TP, Pidsley R, Nisbet J, Glass D, Mangino M, Zhai G, Zhang F, Valdes A, et al: Epigenome-wide scans identify differentially methylated regions for age and age-related phenotypes in a healthy ageing population. PLoS Genet. 2012, 8: e1002629-10.1371\u002Fjournal.pgen.1002629.\nGaragnani P, Bacalini MG, Pirazzini C, Gori D, Giuliani C, Mari D, Di Blasio AM, Gentilini D, Vitale G, Collino S, et al: Methylation of ELOVL2 gene as a new epigenetic marker of age. Aging Cell. 2012, 11: 1132-1134. 10.1111\u002Facel.12005.\nJohansson A, Enroth S, Gyllensten U: Continuous aging of the human DNA Methylome throughout the human lifespan. PLoS One. 2013, 8: e67378-10.1371\u002Fjournal.pone.0067378.\nGeretti E, Shimizu A, Kurschat P, Klagsbrun M: Site-directed mutagenesis in the B-neuropilin-2 domain selectively enhances its affinity to VEGF165, but not to semaphorin 3F. J Biol Chem. 2007, 282: 25698-25707. 10.1074\u002Fjbc.M702942200.\nMiao HQ, Lee P, Lin H, Soker S, Klagsbrun M: Neuropilin-1 expression by tumor cells promotes tumor angiogenesis and progression. Faseb J. 2000, 14: 2532-2539. 10.1096\u002Ffj.00-0250com.\nBagri A, Tessier-Lavigne M, Watts RJ: Neuropilins in tumor biology. Clin Cancer Res. 2009, 15: 1860-1864. 10.1158\u002F1078-0432.CCR-08-0563.\nBielenberg DR, Pettaway CA, Takashima S, Klagsbrun M: Neuropilins in neoplasms: expression, regulation, and function. Exp Cell Res. 2006, 312: 584-593. 10.1016\u002Fj.yexcr.2005.11.024.\nBruder D, Probst-Kepper M, Westendorf AM, Geffers R, Beissert S, Loser K, von Boehmer H, Buer J, Hansen W: Neuropilin-1: a surface marker of regulatory T cells. Eur J Immunol. 2004, 34: 623-630. 10.1002\u002Feji.200324799.\nSarris M, Andersen KG, Randow F, Mayr L, Betz AG: Neuropilin-1 expression on regulatory T cells enhances their interactions with dendritic cells during antigen recognition. Immunity. 2008, 28: 402-413. 10.1016\u002Fj.immuni.2008.01.012.\nRozic G, Lupowitz Z, Zisapel N: Exonal elements and factors involved in the depolarization-induced alternative splicing of neurexin 2. J Mol Neurosci. 2012, 50: 221-233.\nGauthier J, Siddiqui TJ, Huashan P, Yokomaku D, Hamdan FF, Champagne N, Lapointe M, Spiegelman D, Noreau A, Lafreniere RG, et al: Truncating mutations in NRXN2 and ia. Hum Genet. 2011, 130: 563-573. 10.1007\u002Fs00439-011-0975-z.\nPapadopoulou AS, Dooley J, Linterman MA, Pierson W, Ucar O, Kyewski B, Zuklys S, Hollander GA, Matthys P, Gray DH, et al: The thymic epithelial microRNA network elevates the threshold for infection-associated thymic involution via miR-29a mediated suppression of the IFN-alpha receptor. Nat Immunol. 2012, 13: 181-187.\nMa F, Xu S, Liu X, Zhang Q, Xu X, Liu M, Hua M, Li N, Yao H, Cao X: The microRNA miR-29 controls innate and adaptive immune responses to intracellular bacterial infection by targeting interferon-gamma. Nat Immunol. 2011, 12: 861-869. 10.1038\u002Fni.2073.\nSantanam U, Zanesi N, Efanov A, Costinean S, Palamarchuk A, Hagan JP, Volinia S, Alder H, Rassenti L, Kipps T, et al: Chronic lymphocytic leukemia modeled in mouse by targeted miR-29 expression. Proc Natl Acad Sci USA. 2010, 107: 12210-12215. 10.1073\u002Fpnas.1007186107.\nGarzon R, Liu S, Fabbri M, Liu Z, Heaphy CE, Callegari E, Schwind S, Pang J, Yu J, Muthusamy N, et al: MicroRNA-29b induces global DNA hypomethylation and tumor suppressor gene reexpression in acute myeloid leukemia by targeting directly DNMT3A and 3B and indirectly DNMT1. Blood. 2009, 113: 6411-6418. 10.1182\u002Fblood-2008-07-170589.\nFabbri M, Garzon R, Cimmino A, Liu Z, Zanesi N, Callegari E, Liu S, Alder H, Costinean S, Fernandez-Cymering C, et al: MicroRNA-29 family reverts aberrant methylation in lung cancer by targeting DNA methyltransferases 3A and 3B. Proc Natl Acad Sci USA. 2007, 104: 15805-15810. 10.1073\u002Fpnas.0707628104.\nTserel L, Kolde R, Rebane A, Kisand K, Org T, Peterson H, Vilo J, Peterson P: Genome-wide promoter analysis of histone modifications in human monocyte-derived antigen presenting cells. BMC Genomics. 2010, 11: 642-10.1186\u002F1471-2164-11-642.",{"VOID":1572},"10.1186\u002F1742-4933-11-1","2024-04-29T20:13:15.114+00:00","https:\u002F\u002Fimmunityageing.biomedcentral.com\u002Farticles\u002F10.1186\u002F1742-4933-11-1",[1576,1591,1604,1619,1634,1651,1664],{"id":1577,"sortIndex":21,"researcher":20,"roles":1578,"affiliations":1579,"properties":1588,"displayName":1590,"givenName":20,"familyName":20},"eb0a9b9f-cfbb-4882-9141-f0ed2529fed7",[127],[1580],{"id":1581,"sortIndex":21,"affiliation":1582,"properties":20},"24f98393-7930-43e5-86f4-e669503eff7f",{"id":1581,"createTime":20,"updateTime":20,"relativeEntities":1583,"slug":20,"properties":1584,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1587,"statistic":20},[],{"title":1585},{"VI":1586},"Molecular Pathology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia",[],{"title":1589},{"VI":1590},"Liina Tserel",{"id":1592,"sortIndex":91,"researcher":20,"roles":1593,"affiliations":1594,"properties":1601,"displayName":1603,"givenName":20,"familyName":20},"1e96befc-7b4b-4fba-8b5b-6b97763e8e88",[127],[1595],{"id":1581,"sortIndex":21,"affiliation":1596,"properties":20},{"id":1581,"createTime":20,"updateTime":20,"relativeEntities":1597,"slug":20,"properties":1598,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1600,"statistic":20},[],{"title":1599},{"VI":1586},[],{"title":1602},{"VI":1603},"Maia Limbach",{"id":1605,"sortIndex":92,"researcher":20,"roles":1606,"affiliations":1607,"properties":1614,"displayName":1616,"givenName":20,"familyName":20},"fb21a528-0ebf-4861-9b23-f6debf0849f3",[127],[1608],{"id":1581,"sortIndex":21,"affiliation":1609,"properties":20},{"id":1581,"createTime":20,"updateTime":20,"relativeEntities":1610,"slug":20,"properties":1611,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1613,"statistic":20},[],{"title":1612},{"VI":1586},[],{"title":1615,"gsAuthor":1617},{"VI":1616},"Mario 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and obesity are high risk factors for several conditions and diseases. 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Clin Immunol. 2004;113(2):161–71.\nChang LY, Li Y, Kaplan DE. Hepatitis C viraemia reversibly maintains subset of antigen-specific T-bet+ tissue-like memory B cells. J Viral Hepat. 2016;24(5):389–96.\nIllingworth J, Butler NS, Roetynck S, Mwacharo J, Pierce SK, Bejon P, Crompton PD, Marsh K, Ndungu FM. Chronic exposure to Plasmodium falciparum is associated with phenotypic evidence of B and T cell exhaustion. J Immunol. 2013;190(3):1038–47.\nMoir S, Ho J, Malaspina A, Wang W, DiPoto AC, O’Shea MA, Roby G, Kottilil S, Arthos J, Proschan MA, et al. Evidence for HIV-associated B cell exhaustion in a dysfunctional memory B cell compartment in HIV-infected viremic individuals. J Exp Med. 2008;205(8):1797–805.\nFrasca D, Diaz A, Romero M, Blomberg BB. Phenotypic and Functional Characterization of Double Negative B Cells in the Blood of Individuals With Obesity. Front Immunol. 2021;12:616650.\nFrasca D, Diaz A, Romero M, Thaller S, Blomberg BB. Metabolic requirements of human pro-inflammatory B cells in aging and obesity. PLoS ONE. 2019;14(7):e0219545.\nFrasca D, Diaz A, Romero M, Vazquez T, Blomberg BB. Obesity induces pro-inflammatory B cells and impairs B cell function in old mice. Mech Ageing Dev. 2017;162:91–9.\nCarta G, Murru E, Banni S, Manca C. Palmitic Acid: Physiological Role, Metabolism and Nutritional Implications. Front Physiol. 2017;8:902.\nYu Y, Cai Z, Zheng J, Chen J, Zhang X, Huang XF, Li D. Serum levels of polyunsaturated fatty acids are low in Chinese men with metabolic syndrome, whereas serum levels of saturated fatty acids, zinc, and magnesium are high. Nutr Res. 2012;32(2):71–7.",{"VOID":1746},"10.1186\u002Fs12979-022-00301-z","2024-05-10T12:26:32.847+00:00","https:\u002F\u002Fimmunityageing.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12979-022-00301-z",[1750],{"id":1751,"sortIndex":21,"researcher":20,"roles":1752,"affiliations":1753,"properties":1762,"displayName":1764,"givenName":20,"familyName":20},"2bb48e26-fb3c-40ca-a8cb-4619d1b9830c",[127],[1754],{"id":1755,"sortIndex":21,"affiliation":1756,"properties":20},"ba9a846b-4f6e-48e3-b6fd-a9d91208c80d",{"id":1755,"createTime":20,"updateTime":20,"relativeEntities":1757,"slug":20,"properties":1758,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1761,"statistic":20},[],{"title":1759},{"VI":1760},"Department of Microbiology and Immunology and Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, USA",[],{"title":1763},{"VI":1764},"Daniela Frasca",{"url":20,"publisher":1766,"properties":20},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1767,"slug":10,"properties":1768,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1771,"manageAffiliations":1780,"indexDatabases":1791,"url":20,"thumbnailPath":20,"statistic":1806,"gsStatistic":20,"type":96,"analyzePriority":20},[],{"issn":1769,"title":1770},{"VOID":13},{"EN":15},[1772,1776],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1773,"label":1774,"description":1775,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":1777,"label":1778,"description":1779,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":33},{},[1781,1786],{"id":37,"createTime":20,"updateTime":20,"relativeEntities":1782,"slug":20,"properties":1783,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1785,"statistic":20},[],{"title":1784},{"EN":41},[],{"id":44,"createTime":20,"updateTime":20,"relativeEntities":1787,"slug":20,"properties":1788,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1790,"statistic":20},[],{"title":1789},{"EN":48},[],[1792,1799],{"id":52,"indexDatabase":1793,"url":63,"indexYears":64,"academicFieldIds":1798,"indexDatabaseRanking":68},{"id":54,"createTime":20,"updateTime":20,"relativeEntities":1794,"label":1795,"description":1796,"key":60,"publicationTags":1797,"standard":20},[],{"EN":57,"VI":57},{"EN":57,"VI":59},[62],[66,67],{"id":70,"indexDatabase":1800,"url":83,"indexYears":20,"academicFieldIds":1805,"indexDatabaseRanking":20},{"id":72,"createTime":20,"updateTime":20,"relativeEntities":1801,"label":1802,"description":1803,"key":79,"publicationTags":1804,"standard":20},[],{"EN":75,"VI":75},{"EN":77,"VI":78},[81,82],[85,86],{"impactFactor":21,"impactFactorByYear":1807,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":89,"totalPublicationByYear":1808,"totalCitation":21,"totalCitationByYear":1809,"totalCitationPerPublication":21,"totalCitationPerPublicationByYear":1810,"hindexLast5Year":21,"hindex":21},{},{"2005":91,"2010":91,"2014":92,"2020":92,"2022":92,"2023":91,"2024":93},{},{},"2022-10-26",2022,"2026-01-10T12:54:49.328+00:00",[68,81],{"id":1816,"createTime":1817,"updateTime":1818,"relativeEntities":1819,"slug":1820,"properties":1821,"entityType":118,"verifyStatus":119,"verifyTime":1818,"verifyNote":121,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1830,"fullTextUrl":20,"authors":1831,"publicationType":140,"publisherRelationship":1912,"citationCount":20,"citationInfo":20,"publishDate":1962,"publishYear":1963,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":1964,"openAccess":20,"references":20,"isForceReanalyzing":202},"e1053919-de6b-43f6-b4c5-c2ddfcd54fa5","2023-12-21T04:29:43.929+00:00","2025-02-26T01:02:45.615+00:00",[],"Decreased-immunoglobulin-G-in-brain-regions-of-elder-female-APOE4-TR-mice-accompany-with-A%CE%B2-accumulation",{"abstract":1822,"title":1824,"references":1826,"doi":1828},{"EN":1823},"Apolipoprotein E4 (APOE4) and ageing are the most important known risk factors for late-onset Alzheimer’s disease (AD). In the present study, we determined the alterations of IgG, CD19, and Aβ in various brain regions of uninfected male and female APOE3- and APOE4-TR mice at the age of 3 and 10 months to elucidate impacts of AD risk factors on alterations of brain IgG. Positive staining for IgG was distributed across the brain, including neocortex, entorhinal cortex, hippocampus, thalamus and cerebellum. IgG positive staining was mainly located on microglia, but not astrocytes. Some IgG positive neurons were also observed, but only in mediodorsal thalamic nucleus. Compared with APOE3-TR mice, 10-month-old female APOE4-TR mice had lower IgG level in AD susceptible brain regions such as neocortex, entorhinal cortex and hippocampus, but no significant changes in thalamus and cerebellum, two regions nearly intact in AD. In addition, the expression of CD19, a specific marker for mature B cells, was significantly reduced in the hippocampus of 10-month-old female APOE4-TR mice. Although there were no obvious differences in plasma IgG levels between APOE4- and age matched female APOE3-TR mice, significant decreased B cell amount in blood of 10-month-old female APOE4-TR mice have also been found. Moreover, more obvious positive staining for Aβ was observed in the cortex of 10-month-old female APOE4-TR mice than other groups. Our study demonstrated that AD risk factors were associated with IgG alterations in various brain regions, which might result from the defects of humoral immunity and lead to the impairment of IgG-mediated clearance of Aβ by microglia, therefore facilitated AD progression.",{"EN":1825},"Decreased immunoglobulin G in brain regions of elder female APOE4-TR mice accompany with Aβ accumulation",{"VOID":1827},"Dong S, Duan Y, Hu Y, Zhao Z. Advances in the pathogenesis of Alzheimer's disease: a re-evaluation of amyloid cascade hypothesis. Transl Neurodegener. 2012;1(1):18.\n2016 Alzheimer's disease facts and figures. Alzheimer's & dementia : the journal of the Alzheimer's Association 2016;12(4):459–509.\nKarlamangla AS, Lachman ME, Han W, Huang M, Greendale GA. Evidence for cognitive aging in midlife women: study of Women's health across the nation. PLoS One. 2017;12(1):e0169008.\nCorder EH, Saunders AM, Strittmatter WJ, Schmechel DE, Gaskell PC, Small GW, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families. Science. 1993;261(5123):921–3.\nCacciottolo M, Christensen A, Moser A, Liu J, Pike CJ, Smith C, et al. The APOE4 allele shows opposite sex bias in microbleeds and Alzheimer's disease of humans and mice. Neurobiol Aging. 2016;37:47–57.\nHuang YA, Zhou B, Wernig M, Sudhof TC. ApoE2, ApoE3, and ApoE4 differentially stimulate APP transcription and Abeta secretion. Cell. 2017;168(3):427–41.e21.\nCastellano JM, Kim J, Stewart FR, Jiang H, DeMattos RB, Patterson BW, et al. Human apoE isoforms differentially regulate brain amyloid-beta peptide clearance. Sci Transl Med. 2011;3(89):89ra57.\nVerghese PB, Castellano JM, Garai K, Wang Y, Jiang H, Shah A, et al. ApoE influences amyloid-β (Aβ) clearance despite minimal apoE\u002FAβ association in physiological conditions. Proc Natl Acad Sci U S A. 2013;110(19):E1807–E16.\nFouquet M, Besson FL, Gonneaud J, La Joie R, Chetelat G. Imaging brain effects of APOE4 in cognitively normal individuals across the lifespan. Neuropsychol Rev. 2014;24(3):290–9.\nTakata K, Kitamura Y, Yanagisawa D, Morikawa S, Morita M, Inubushi T, et al. Microglial transplantation increases amyloid-beta clearance in Alzheimer model rats. FEBS Lett. 2007;581(3):475–8.\nPan XD, Zhu YG, Lin N, Zhang J, Ye QY, Huang HP, et al. Microglial phagocytosis induced by fibrillar beta-amyloid is attenuated by oligomeric beta-amyloid: implications for Alzheimer's disease. Mol Neurodegener. 2011;6:45.\nMagga J, Puli L, Pihlaja R, Kanninen K, Neulamaa S, Malm T, et al. Human intravenous immunoglobulin provides protection against Aβ toxicity by multiple mechanisms in a mouse model of Alzheimer's disease. J Neuroinflammation. 2010;7(1):90.\nRelkin N. Intravenous immunoglobulin for Alzheimer's disease. Clin Exp Immunol. 2014;178(Suppl 1):27–9.\nRies M, Sastre M. Mechanisms of Abeta clearance and degradation by glial cells. Front Aging Neurosci. 2016;8:160.\nSudduth TL, Greenstein A, Wilcock DM. Intracranial injection of Gammagard, a human IVIg, modulates the inflammatory response of the brain and lowers Abeta in APP\u002FPS1 mice along a different time course than anti-Abeta antibodies. J Neurosci. 2013;33(23):9684–92.\nCounts SE, Ray B, Mufson EJ, Perez SE, He B, Lahiri DK. Intravenous immunoglobulin (IVIG) treatment exerts antioxidant and neuropreservatory effects in preclinical models of Alzheimer's disease. J Clin Immunol. 2014;34(Suppl 1):S80–5.\nRelkin N. Clinical trials of intravenous immunoglobulin for Alzheimer's disease. J Clin Immunol. 2014;34(Suppl 1):S74–9.\nRelkin NR, Thomas RG, Rissman RA, Brewer JB, Rafii MS, van Dyck CH, et al. A phase 3 trial of IV immunoglobulin for Alzheimer disease. Neurology. 2017;88(18):1768–75.\nSalloway S, Sperling R, Gilman S, Fox NC, Blennow K, Raskind M, et al. A phase 2 multiple ascending dose trial of bapineuzumab in mild to moderate Alzheimer disease. Neurology. 2009;73(24):2061–70.\nKnight EM, Gandy S. Immunomodulation and AD – down but not out. J Clin Immunol. 2014;34(1):70–3.\nZhou Y, Zhao W, Al-Muhtasib N, Rebeck GW. APOE genotype alters immunoglobulin subtypes in Knock-in mice. J Alzheimers Dis. 2015;46(2):365–74.\nZhao W, Dumanis SB, Tamboli IY, Rodriguez GA, Jo Ladu M, Moussa CE, et al. Human APOE genotype affects intraneuronal Abeta1-42 accumulation in a lentiviral gene transfer model. Hum Mol Genet. 2014;23(5):1365–75.\nZhao W, Zhang J, Davis EG, Rebeck GW. Aging reduces glial uptake and promotes extracellular accumulation of Abeta from a lentiviral vector. Front Aging Neurosci. 2014;6:210.\nSullivan PM, Mezdour H, Aratani Y, Knouff C, Najib J, Reddick RL, et al. Targeted replacement of the mouse apolipoprotein E gene with the common human APOE3 allele enhances diet-induced hypercholesterolemia and atherosclerosis. J Biol Chem. 1997;272(29):17972–80.\nHixson JE, Vernier DT. Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhaI. J Lipid Res. 1990;31(3):545–8.\nZechariah A, ElAli A, Hermann DM. Combination of tissue-plasminogen activator with erythropoietin induces blood-brain barrier permeability, extracellular matrix disaggregation, and DNA fragmentation after focal cerebral ischemia in mice. Stroke. 2010;41(5):1008–12.\nZhang X, Chen XP, Lin JB, Xiong Y, Liao WJ, Wan Q. Effect of enriched environment on angiogenesis and neurological functions in rats with focal cerebral ischemia. Brain Res. 2017;1655:176–85.\nGould E, Woolley CS, McEwen BS. The hippocampal formation: morphological changes induced by thyroid, gonadal and adrenal hormones. Psychoneuroendocrinology. 1991;16(1–3):67–84.\nLi XB, Inoue T, Nakagawa S, Koyama T. Effect of mediodorsal thalamic nucleus lesion on contextual fear conditioning in rats. Brain Res. 2004;1008(2):261–72.\nHeo Y, Zhang Y, Gao D, Miller VM, Lawrence DA. Aberrant immune responses in a mouse with behavioral disorders. PLoS One. 2011;6(7):e20912.\nMarsh SE, Abud EM, Lakatos A, Karimzadeh A, Yeung ST, Davtyan H, et al. The adaptive immune system restrains Alzheimer's disease pathogenesis by modulating microglial function. Proc Natl Acad Sci U S A. 2016;113(9):E1316–25.\nGlass LJ, Sinclair D, Boerrigter D, Naude K, Fung SJ, Brown D, et al. Brain antibodies in the cortex and blood of people with schizophrenia and controls. Transl Psychiatry. 2017;7(8):e1192.\nDeane R, Sagare A, Hamm K, Parisi M, LaRue B, Guo H, et al. IgG-assisted age-dependent clearance of Alzheimer's amyloid beta peptide by the blood-brain barrier neonatal fc receptor. J Neurosci. 2005;25(50):11495–503.\nBake S, Friedman J, Sohrabji F. Reproductive age-related changes in the blood brain barrier: expression of IgG and tight junction proteins. Microvasc Res. 2009;78(3):413–24.\nIngalhalikar M, Smith A, Parker D, Satterthwaite TD, Elliott MA, Ruparel K, et al. Sex differences in the structural connectome of the human brain. Proc Natl Acad Sci. 2014;111(2):823–8.\nVerthelyi D. Sex hormones as immunomodulators in health and disease. Int Immunopharmacol. 2001;1(6):983–93.\nAhmed SA, Talal N. Sex hormones and the immune system-part 2. Animal data. Baillieres Clin Rheumatol. 1990;4(1):13–31.\nFernandez-Vizarra P, Lopez-Franco O, Mallavia B, Higuera-Matas A, Lopez-Parra V, Ortiz-Munoz G, et al. Immunoglobulin G fc receptor deficiency prevents Alzheimer-like pathology and cognitive impairment in mice. Brain : a journal of neurology. 2012;135(Pt 9):2826–37.\nHuang J, Sun X, Mao Y, Zhu X, Zhang P, Zhang L, et al. Expression of immunoglobulin gene with classical V-(D)-J rearrangement in mouse brain neurons. Int J Biochem Cell Biol. 2008;40(8):1604–15.\nLovato L, Willis SN, Rodig SJ, Caron T, Almendinger SE, Howell OW, et al. Related B cell clones populate the meninges and parenchyma of patients with multiple sclerosis. Brain : a journal of neurology. 2011;134(Pt 2):534–41.\nAlter A, Duddy M, Hebert S, Biernacki K, Prat A, Antel JP, et al. Determinants of human B cell migration across brain endothelial cells. J Immunol. 2003;170(9):4497–505.\nZhang J, Niu N, Li B, McNutt MA. Neuron-derived IgG protects neurons from complement-dependent cytotoxicity. J Histochem Cytochem. 2013;61(12):869–79.\nZhang J, Niu N, Wang M, McNutt MA, Zhang D, Zhang B, et al. Neuron-derived IgG protects dopaminergic neurons from insult by 6-OHDA and activates microglia through the FcγR i and TLR4 pathways. Int J Biochem Cell Biol. 2013;45(8):1911–20.\nLouveau A, Smirnov I, Keyes TJ, Eccles JD, Rouhani SJ, Peske JD, et al. Structural and functional features of central nervous system lymphatic vessels. Nature. 2015;523(7560):337–41.\nAnthony IC, Crawford DH, Bell JE. B lymphocytes in the normal brain: contrasts with HIV-associated lymphoid infiltrates and lymphomas. Brain : a journal of neurology. 2003;126(Pt 5):1058–67.\nDoyle KP, Buckwalter MS. Does B lymphocyte-mediated autoimmunity contribute to post-stroke dementia? Brain Behav Immun. 2017;64:1–8.\nGylys KH, Fein JA, Tan AM, Cole GM. Apolipoprotein E enhances uptake of soluble but not aggregated amyloid-β protein into synaptic terminals. J Neurochem. 2003;84(6):1442–51.\nIstrin G, Bosis E, Solomon B. Intravenous immunoglobulin enhances the clearance of fibrillar amyloid-beta peptide. J Neurosci Res. 2006;84(2):434–43.\nFu R, Shen Q, Xu P, Luo JJ, Tang Y. Phagocytosis of microglia in the central nervous system diseases. Mol Neurobiol. 2014;49(3):1422–34.",{"VOID":1829},"10.1186\u002Fs12979-018-0142-7","https:\u002F\u002Fimmunityageing.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12979-018-0142-7",[1832,1847,1860,1873,1886,1899],{"id":1833,"sortIndex":21,"researcher":20,"roles":1834,"affiliations":1835,"properties":1844,"displayName":1846,"givenName":20,"familyName":20},"ddbad77e-a8c9-4b84-b99d-b816274984ec",[127],[1836],{"id":1837,"sortIndex":21,"affiliation":1838,"properties":20},"41d4184c-61db-4755-8153-8c8dd9da2fbc",{"id":1837,"createTime":20,"updateTime":20,"relativeEntities":1839,"slug":20,"properties":1840,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1843,"statistic":20},[],{"title":1841},{"EN":1842},"School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China",[],{"title":1845},{"VI":1846},"Lihang 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               \u003Cjats:title>Background\u003C\u002Fjats:title>\n                \u003Cjats:p>Immunosenescence is a complex process characterized by an age-related remodelling of immune system. The prominent effects of the immunosenescence process is the thymic involution and, consequently, the decreased numbers and functions of T cells. Since thymic involution results in a collapse of the T-cell receptor (TCR) repertoire, a reliable biomarker of its activity is represented by the quantification of signal joint T-cell receptor rearrangement excision circles (sjTRECs) levels. Although it is reasonable to think that thymic function could play a crucial role on elderly survival, only a few studies investigated the relationship between an accurate measurement of human thymic function and survival at old ages.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Methods and findings\u003C\u002Fjats:title>\n                \u003Cjats:p>By quantifying the amount sjTRECs by real-time polymerase chain reaction (PCR), the decrease in thymic output in 241 nursing home residents from Calabria (Southern Italy) was evaluated to investigate the relationship between thymic function and survival at old ages. We found that low sjTREC levels were associated with a significant increased risk of mortality at older ages. Nursing home residents with lower sjTREC exhibit a near 2-fold increase in mortality risk compared to those with sjTREC levels in a normal range.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Conclusion\u003C\u002Fjats:title>\n                \u003Cjats:p>Thymic function failure is an independent predictor of mortality among elderly nursing home residents. sjTREC represents a biomarker of effective ageing as its blood levels could anticipate individuals at high risk of negative health outcomes. The identification of these subjects is crucial to manage older people’s immune function and resilience, such as, for instance, to plan more efficient vaccinal campaigns in older populations.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>",{"EN":1977},"Thymic function and survival at advance ages in nursing home residents from Southern 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