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of toll-like receptors in neonatal sepsis, Pediatr Res, 58, 654, 10.1203\u002F01.PDR.0000180544.02537.FD",{"doi":526},"10.1203\u002F01.PDR.0000180544.02537.FD",{"id":24,"text":528,"url":24,"identifiers":529},"Canto, 2006, TNF alpha production to TLR2 ligands in active IBD patients, Clin Immunol, 119, 156, 10.1016\u002Fj.clim.2005.12.005",{"doi":530},"10.1016\u002Fj.clim.2005.12.005",{"id":24,"text":532,"url":24,"identifiers":533},"Gagro, 2004, Increased Toll-like receptor 4 expression in infants with respiratory syncytial virus bronchiolitis, Clin Exp Immunol, 135, 267, 10.1111\u002Fj.1365-2249.2004.02364.x",{"doi":534},"10.1111\u002Fj.1365-2249.2004.02364.x",{"id":24,"text":536,"url":24,"identifiers":537},"Pons, 2006, Expression of Toll-like receptor 2 is up-regulated in monocytes from patients with chronic obstructive pulmonary disease, Respir Res, 7, 64, 10.1186\u002F1465-9921-7-64",{"doi":538},"10.1186\u002F1465-9921-7-64",{"id":24,"text":540,"url":24,"identifiers":541},"Lee, 2006, 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have previously reported the presence of marked immune dysregulation with a dominant Th2 profile, in a population of Ethiopian immigrants (ETH) in Israel heavily infected with helminths. In order to characterize better this immune dysregulation we studied by flow cytometry the expression of several activation markers on peripheral T cell populations, and lymphocyte apoptosis, in blood samples obtained from 63 ‘new’ ETH (recently arrived), 18 ‘old’ ETH (> 5 years since immigration) and 34 non-Ethiopian Israelis. The main findings in the ‘new’ ETH group in comparison with the non-Ethiopian controls were: (i) decreased CD4 and increased CD8 lymphocyte counts; (ii) elevated levels of activated T cells (CD3, CD4 and CD8) expressing HLA-DR; (iii) decreased levels of ‘naive’ CD4+ cells (CD45RA+), with increased levels of ‘memory’ CD4+ cells (CD45RO+); (iv) decreased numbers of CD28+ CD8+ lymphocytes; (v) marked increase in lymphocyte apoptosis. These T cell alterations and activation profile remained unchanged in 10 ‘new’ ETH in whom the helminth infections persisted for 6–11 months. In contrast, in 18 ‘old’ ETH, without helminth infections, the T cell activation profile was within the normal range. These findings suggest that chronic helminth infections may have a profound effect on the immune system of the host that disappears after eradication of these infections and adjustment to the new environment. 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Variability of levels of peripheral leukocytes, lymphocyte subsets and beta-2 microglobulin (B-2M) in HIV-1 seronegative adults. 3rd Federation of African Immunological Societies Congress (FAIS), 9-13 March 1997 ; Cape Town, South Africa. 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10.4269\u002Fajtmh.1997.56.522",{"doi":990},"10.4269\u002Fajtmh.1997.56.522",{"id":992,"createTime":993,"updateTime":994,"relativeEntities":995,"slug":996,"properties":997,"entityType":182,"verifyStatus":183,"verifyTime":1014,"verifyNote":184,"languages":1015,"translateLanguages":24,"viewCount":25,"primaryUrl":1016,"fullTextUrl":24,"authors":1017,"publicationType":389,"publisherRelationship":1118,"citationCount":25,"citationInfo":1173,"publishDate":1176,"publishYear":1174,"citationAnalyzeStatus":23,"lastCitationAnalyze":994,"indexDatabases":1177,"openAccess":24,"references":1178,"isForceReanalyzing":570},"e633dc67-205e-4211-8051-ebc6672186be","2025-01-06T12:00:51.668+00:00","2025-07-13T14:58:15.945+00:00",[],"Enhanced-formation-and-impaired-degradation-of-neutrophil-extracellular-traps-in-dermatomyositis-and-polymyositis-a-potential-contributor-to-interstitial-lung-disease-complications",{"mag":998,"gsPaper":1000,"pmc":1002,"openalex":1004,"abstract":1006,"title":1008,"pm":1010,"doi":1012},{"VOID":999},"1516247662",{"VOID":1001},"[\"3345001026813335728\"]",{"VOID":1003},"4089162",{"VOID":1005},"W1516247662",{"EN":1007},"\u003Cjats:title>Summary\u003C\u002Fjats:title>\n               \u003Cjats:p>Dermatomyositis (DM) and polymyosits (PM) are systemic autoimmune diseases whose pathogeneses remain unclear. Neutrophil extracellular traps (NETs) are reputed to play an important role in the pathogenesis of autoimmune diseases. This study tests the hypothesis that NETs may be pathogenic in DM\u002FPM. Plasma samples from 97 DM\u002FPM patients (72 DM, 25 PM) and 54 healthy controls were tested for the capacities to induce and degrade NETs. Plasma DNase I activity was tested to further explore possible reasons for the incomplete degradation of NETs. Results from 35 DM patients and seven PM patients with interstitial lung disease (ILD) were compared with results from DM\u002FPM patients without ILD. Compared with control subjects, DM\u002FPM patients exhibited a significantly enhanced capacity for inducing NETs, which was supported by elevated levels of plasma LL-37 and circulating cell-free DNA (cfDNA) in DM\u002FPM. NETs degradation and DNase I activity were also decreased significantly in DM\u002FPM patients and were correlated positively. Moreover, DM\u002FPM patients with ILD exhibited the lowest NETs degradation in vitro due to the decrease in DNase I activity. DNase I activity in patients with anti-Jo-1 antibodies was significantly lower than in patients without. Glucocorticoid therapy seems to improve DNase I activity. Our findings demonstrate that excessively formed NETs cannot be degraded completely because of decreased DNase I activity in DM\u002FPM patients, especially in patients with ILD, suggesting that abnormal regulation of NETs may be involved in the pathogenesis of DM\u002FPM and could be one of the factors that initiate and aggravate ILD.\u003C\u002Fjats:p>",{"EN":1009},"Enhanced formation and impaired degradation of neutrophil extracellular traps in dermatomyositis and polymyositis: a potential contributor to interstitial lung disease complications",{"VOID":1011},"24611519",{"VOID":1013},"10.1111\u002Fcei.12319","2025-01-06T12:00:51.667+00:00",[186],"https:\u002F\u002Facademic.oup.com\u002Fcei\u002Farticle\u002F177\u002F1\u002F134\u002F6421365",[1018,1037,1054,1071,1086,1103],{"id":1019,"sortIndex":25,"researcher":24,"roles":1020,"affiliations":1021,"properties":1030,"displayName":1034,"givenName":24,"familyName":24},"73034eae-26e8-4fd5-b30a-8257c6239fdf",[],[1022],{"id":1023,"sortIndex":25,"affiliation":1024,"properties":24},"1aab2e7c-8a85-481f-9a04-46ef82b4f21e",{"id":1023,"createTime":24,"updateTime":24,"relativeEntities":1025,"slug":24,"properties":1026,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1029,"statistic":24},[],{"title":1027},{"VI":1028},"Department of Rheumatology, China-Japan Friendship Hospital, Beijing, China",[],{"orcid":1031,"title":1033,"openalex":1035},{"VOID":1032},"https:\u002F\u002Forcid.org\u002F0000-0003-1565-1431",{"EN":1034},"Sigong Zhang",{"VOID":1036},"A5102773477",{"id":1038,"sortIndex":104,"researcher":24,"roles":1039,"affiliations":1040,"properties":1047,"displayName":1051,"givenName":24,"familyName":24},"b70e90c1-2c0d-4e08-9a70-8435d40b442e",[],[1041],{"id":1023,"sortIndex":25,"affiliation":1042,"properties":24},{"id":1023,"createTime":24,"updateTime":24,"relativeEntities":1043,"slug":24,"properties":1044,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1046,"statistic":24},[],{"title":1045},{"VI":1028},[],{"orcid":1048,"title":1050,"openalex":1052},{"VOID":1049},"https:\u002F\u002Forcid.org\u002F0000-0001-5425-6157",{"EN":1051},"Xiaoming Shu",{"VOID":1053},"A5050860854",{"id":1055,"sortIndex":114,"researcher":24,"roles":1056,"affiliations":1057,"properties":1064,"displayName":1068,"givenName":24,"familyName":24},"bb5b1729-0e2a-47c8-800c-644227e52793",[],[1058],{"id":1023,"sortIndex":25,"affiliation":1059,"properties":24},{"id":1023,"createTime":24,"updateTime":24,"relativeEntities":1060,"slug":24,"properties":1061,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1063,"statistic":24},[],{"title":1062},{"VI":1028},[],{"orcid":1065,"title":1067,"openalex":1069},{"VOID":1066},"https:\u002F\u002Forcid.org\u002F0000-0001-5225-6284",{"EN":1068},"Xiaowen Tian",{"VOID":1070},"A5018907801",{"id":1072,"sortIndex":102,"researcher":24,"roles":1073,"affiliations":1074,"properties":1081,"displayName":1083,"givenName":24,"familyName":24},"b8b88f35-8a6a-4b3c-a1bd-a6dac4ee408e",[],[1075],{"id":1023,"sortIndex":25,"affiliation":1076,"properties":24},{"id":1023,"createTime":24,"updateTime":24,"relativeEntities":1077,"slug":24,"properties":1078,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1080,"statistic":24},[],{"title":1079},{"VI":1028},[],{"title":1082,"openalex":1084},{"EN":1083},"F. 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2011, Pathogenesis, classification and treatment of inflammatory myopathies, Nat Rev Rheumatol, 7, 297, 10.1038\u002Fnrrheum.2011.39",{"doi":1182},"10.1038\u002Fnrrheum.2011.39",{"id":24,"text":1184,"url":24,"identifiers":1185},"Dalakas, 2012, Pathogenesis and therapies of immune-mediated myopathies, Autoimmun Rev, 11, 203, 10.1016\u002Fj.autrev.2011.05.013",{"doi":1186},"10.1016\u002Fj.autrev.2011.05.013",{"id":24,"text":1188,"url":24,"identifiers":1189},"Danoff, 2011, The lung as a possible target for the immune reaction in myositis, Arthritis Res Ther, 13, 230, 10.1186\u002Far3347",{"doi":1190},"10.1186\u002Far3347",{"id":24,"text":1192,"url":24,"identifiers":1193},"Hirakata, 2000, Interstitial lung disease in polymyositis and dermatomyositis, Curr Opin Rheumatol, 12, 501, 10.1097\u002F00002281-200011000-00005",{"doi":1194},"10.1097\u002F00002281-200011000-00005",{"id":24,"text":1196,"url":24,"identifiers":1197},"Cheng, 2013, NET balancing: a problem in inflammatory lung diseases, Front Immunol, 4, 1, 10.3389\u002Ffimmu.2013.00001",{"doi":1198},"10.3389\u002Ffimmu.2013.00001",{"id":24,"text":1200,"url":24,"identifiers":1201},"Khandpur, 2013, NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis, Sci Transl Med, 5, 178ra40, 10.1126\u002Fscitranslmed.3005580",{"doi":1202},"10.1126\u002Fscitranslmed.3005580",{"id":24,"text":1204,"url":24,"identifiers":1205},"Keshari, 2012, Cytokines induced neutrophil extracellular traps formation: implication for the inflammatory disease condition, PLOS ONE, 7, e48111, 10.1371\u002Fjournal.pone.0048111",{"doi":1206},"10.1371\u002Fjournal.pone.0048111",{"id":24,"text":1208,"url":24,"identifiers":1209},"Downey, 2009, Neutrophils in cystic fibrosis, Thorax, 64, 81, 10.1136\u002Fthx.2007.082388",{"doi":1210},"10.1136\u002Fthx.2007.082388",{"id":24,"text":1212,"url":24,"identifiers":1213},"Hakkim, 2010, Impairment of neutrophil extracellular trap degradation is associated with lupus nephritis, Proc Natl Acad Sci USA, 107, 9813, 10.1073\u002Fpnas.0909927107",{"doi":1214},"10.1073\u002Fpnas.0909927107",{"id":24,"text":1216,"url":24,"identifiers":1217},"Villanueva, 2011, Netting neutrophils induce endothelial damage, infiltrate tissues, and expose immunostimulatory molecules in systemic lupus erythematosus, J Immunol, 187, 538, 10.4049\u002Fjimmunol.1100450",{"doi":1218},"10.4049\u002Fjimmunol.1100450",{"id":24,"text":1220,"url":24,"identifiers":1221},"Leffler, 2012, Neutrophil extracellular traps that are not degraded in systemic lupus erythematosus activate complement exacerbating the disease, J Immunol, 188, 3522, 10.4049\u002Fjimmunol.1102404",{"doi":1222},"10.4049\u002Fjimmunol.1102404",{"id":24,"text":1224,"url":24,"identifiers":1225},"Kessenbrock, 2009, Netting neutrophils in autoimmune small-vessel vasculitis, Nat Med, 15, 623, 10.1038\u002Fnm.1959",{"doi":1226},"10.1038\u002Fnm.1959",{"id":24,"text":1228,"url":24,"identifiers":1229},"Manzenreiter, 2012, Ultrastructural characterization of cystic fibrosis sputum using atomic force and scanning electron microscopy, J Cyst Fibros, 11, 84, 10.1016\u002Fj.jcf.2011.09.008",{"doi":1230},"10.1016\u002Fj.jcf.2011.09.008",{"id":24,"text":1232,"url":24,"identifiers":1233},"Thomas, 2012, Extracellular DNA traps are associated with the pathogenesis of TRALI in humans and mice, Blood, 119, 6335, 10.1182\u002Fblood-2012-01-405183",{"doi":1234},"10.1182\u002Fblood-2012-01-405183",{"id":24,"text":1236,"url":24,"identifiers":1237},"Caudrillier, 2012, Platelets induce neutrophil extracellular traps in transfusion-related acute lung injury, J Clin Invest, 122, 2661, 10.1172\u002FJCI61303",{"doi":1238},"10.1172\u002FJCI61303",{"id":24,"text":1240,"url":24,"identifiers":1241},"Brinkmann, 2004, Neutrophil extracellular traps kill bacteria, Science, 303, 1532, 10.1126\u002Fscience.1092385",{"doi":1242},"10.1126\u002Fscience.1092385",{"id":24,"text":1244,"url":24,"identifiers":1245},"Fuchs, 2007, Novel cell death program leads to neutrophil extracellular traps, J Cell Biol, 176, 231, 10.1083\u002Fjcb.200606027",{"doi":1246},"10.1083\u002Fjcb.200606027",{"id":24,"text":1248,"url":24,"identifiers":1249},"Liu, 2012, Specific post-translational histone modifications of neutrophil extracellular traps as immunogens and potential targets of lupus autoantibodies, Arthritis Res Ther, 14, R25, 10.1186\u002Far3707",{"doi":1250},"10.1186\u002Far3707",{"id":24,"text":1252,"url":24,"identifiers":1253},"Saffarzadeh, 2012, Neutrophil extracellular traps directly induce epithelial and endothelial cell death: a predominant role of histones, PLOS ONE, 7, e32366, 10.1371\u002Fjournal.pone.0032366",{"doi":1254},"10.1371\u002Fjournal.pone.0032366",{"id":24,"text":1256,"url":24,"identifiers":1257},"Xu, 2009, Extracellular histones are major mediators of death in sepsis, Nat Med, 15, 1318, 10.1038\u002Fnm.2053",{"doi":1258},"10.1038\u002Fnm.2053",{"id":24,"text":1260,"url":24,"identifiers":1261},"Garcia-Romo, 2011, Netting neutrophils are major inducers of type I IFN production in pediatric systemic lupus erythematosus, Sci Transl Med, 3, 73ra20, 10.1126\u002Fscitranslmed.3001201",{"doi":1262},"10.1126\u002Fscitranslmed.3001201",{"id":24,"text":1264,"url":24,"identifiers":1265},"Lande, 2011, Neutrophils activate plasmacytoid dendritic cells by releasing self-DNA-peptide complexes in systemic lupus erythematosus, Sci Transl Med, 3, 73ra19, 10.1126\u002Fscitranslmed.3001180",{"doi":1266},"10.1126\u002Fscitranslmed.3001180",{"id":24,"text":1268,"url":24,"identifiers":1269},"Bosch, 2011, Systemic lupus erythematosus and the neutrophil, N Engl J Med, 365, 758, 10.1056\u002FNEJMcibr1107085",{"doi":1270},"10.1056\u002FNEJMcibr1107085",{"id":24,"text":1272,"url":24,"identifiers":1273},"Bohan, 1975, Polymyositis and dermatomyositis (first of two parts), N Engl J Med, 292, 344, 10.1056\u002FNEJM197502132920706",{"doi":1274},"10.1056\u002FNEJM197502132920706",{"id":24,"text":1276,"url":24,"identifiers":1277},"Bohan, 1975, Polymyositis and dermatomyositis (second of two parts), N Engl J Med, 292, 403, 10.1056\u002FNEJM197502202920807",{"doi":1278},"10.1056\u002FNEJM197502202920807",{"id":24,"text":1280,"url":24,"identifiers":1281},"Rider, 2011, Measures of adult and juvenile dermatomyositis, polymyositis, and inclusion body myositis: Physician and Patient\u002FParent Global Activity, Manual Muscle Testing (MMT), Health Assessment Questionnaire (HAQ)\u002FChildhood Health Assessment Questionnaire (C-HAQ), Childhood Myositis Assessment Scale (CMAS), Myositis Disease Activity Assessment Tool (MDAAT), Disease Activity Score (DAS), Short Form 36 (SF-36), Child Health Questionnaire (CHQ), physician global damage, Myositis Damage Index (MDI), Quantitative Muscle Testing (QMT), Myositis Functional Index-2 (FI-2), Myositis Activities Profile (MAP), Inclusion Body Myositis Functional Rating Scale (IBMFRS), Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI), Cutaneous Assessment Tool (CAT), Dermatomyositis Skin Severity Index (DSSI), Skindex, and Dermatology Life Quality Index (DLQI), Arthritis Care Res (Hoboken), 63, S118, 10.1002\u002Facr.20532",{"doi":1282},"10.1002\u002Facr.20532",{"id":24,"text":1284,"url":24,"identifiers":1285},"Macanovic, 1997, Measurement of deoxyribonuclease I (DNase) in the serum and urine of systemic lupus erythematosus (SLE)-prone NZB\u002FNZW mice by a new radial enzyme diffusion assay, Clin Exp Immunol, 108, 220, 10.1046\u002Fj.1365-2249.1997.3571249.x",{"doi":1286},"10.1046\u002Fj.1365-2249.1997.3571249.x",{"id":24,"text":1288,"url":24,"identifiers":1289},"Margraf, 2008, Neutrophil-derived circulating free DNA (cf-DNA\u002FNETS): a potential prognostic marker for posttraumatic development of inflammatory second hit and sepsis, Shock, 30, 352, 10.1097\u002FSHK.0b013e31816a6bb1",{"doi":1290},"10.1097\u002FSHK.0b013e31816a6bb1",{"id":1292,"createTime":1293,"updateTime":1294,"relativeEntities":1295,"slug":1296,"properties":1297,"entityType":182,"verifyStatus":183,"verifyTime":1293,"verifyNote":184,"languages":1316,"translateLanguages":1317,"viewCount":25,"primaryUrl":1319,"fullTextUrl":24,"authors":1320,"publicationType":389,"publisherRelationship":1404,"citationCount":1458,"citationInfo":1459,"publishDate":1462,"publishYear":1460,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1463,"openAccess":24,"references":1464,"isForceReanalyzing":570},"5c124326-69af-4037-b39a-de636359dec1","2024-12-03T12:19:14.730+00:00","2025-02-11T00:02:33.509+00:00",[],"CD8-lymphocytosis-in-primary-cytomegalovirus-CMV-infection-of-allograft-recipients-expansion-of-an-uncommon-CD8-CD57-subset-and-its-progressive-replacement-by-CD8-CD57-T-cells",{"mag":1298,"keywords":1300,"pmc":1302,"openalex":1304,"abstract":1306,"title":1309,"pm":1312,"doi":1314},{"VOID":1299},"2149299386",{"VI":1301},"",{"VOID":1303},"1535098",{"VOID":1305},"W2149299386",{"EN":1307,"VI":1308},"\u003Cjats:title>SUMMARY\u003C\u002Fjats:title>\u003Cjats:p>Allograft recipients undergoing eytomegalovirus infection present increased proportions of circulating CD8+ lymphocytes. A longitudinal study of 11 kidney and five liver allograft recipients with primary CMV infection but no other etiological factor of graft dysfunction revealed selective imbalances of peripheral blood CDS+ T cell subsets. Initially, CMV viraemia is associated with elevated CDS+ bright T cell numbers and T cell activation. Activation markers fall to normal when viral cultures become negative (before the end of the first month). During the second to sixth month, most (12\u002F16) patients keep up high CD8+ T cell counts (1050-2900 CD8+ cells\u002Fmm3), comprising an uncommon CD8+ T cell subset, as 45-73% of CD8+bright lymphocytes were CD3+ and TCRαβ+, but were not stained by anti-CD28, CDIIb, CD16. CD56. and CD57 antibody. Unexpectedly, CD8+CD57+ T cells, a hallmark of CMV infection, do not appear until the second to sixth month of primary CMV infection, and their numbers increase progressively thereafter. They become the predominant CD8+ T cell subset after 6 months of infection and their persistence for several (up to 4) years is strongly correlated (r = 0-87) with expansion of CD8+ cells. By analysis with MoAbs, there was no bias towards the use of particular TCR-Vβ gene families al any time of primary CMV infection. Persistence of CD8 lymphocytosis is thus directly related to the rate of expansion of an uncommon CD8+ CD57- subset and its progressive replacement by CD8+ CD57+ T cells that are chronically elicited by CMV.\u003C\u002Fjats:p>","\u003Cjats:title>TÓM TẮT\u003C\u002Fjats:title>\u003Cjats:p>Các người nhận ghép tạng bị nhiễm virus cytomegalovirus (CMV) có tỷ lệ tế bào lympho CD8+ tuần hoàn tăng lên. Một nghiên cứu theo chiều dọc trên 11 người nhận ghép thận và 5 người nhận ghép gan có nhiễm CMV nguyên phát nhưng không có yếu tố nguyên nhân nào khác gây ra rối loạn chức năng ghép cho thấy sự mất cân bằng chọn lọc của các phân nhóm T tế bào CD8+ trong máu ngoại biên. Ban đầu, sự nhiễm CMV có viremia đi kèm với sự gia tăng số lượng T tế bào CD8+ sáng và hoạt hóa T tế bào. Các dấu hiệu hoạt hóa trở về mức bình thường khi nuôi cấy virus trở thành âm tính (trước khi kết thúc tháng đầu tiên). Trong khoảng thời gian từ tháng thứ hai đến tháng thứ sáu, đa số (12\u002F16) bệnh nhân duy trì số lượng T tế bào CD8+ cao (1050-2900 tế bào CD8+\u002Fmm3), bao gồm một phân nhóm tế bào CD8+ không phổ biến, khi 45-73% lympho CD8+ sáng là CD3+ và TCRαβ+, nhưng không bị nhuộm bởi kháng thể anti-CD28, CDIIb, CD16, CD56 và CD57. Đáng ngạc nhiên là, tế bào T CD8+CD57+, một dấu hiệu đặc trưng của nhiễm CMV, không xuất hiện cho đến tháng thứ hai đến tháng thứ sáu của nhiễm CMV nguyên phát, và số lượng của chúng tăng dần sau đó. Chúng trở thành phân nhóm tế bào T CD8+ chủ yếu sau 6 tháng nhiễm bệnh và sự tồn tại của chúng trong vài (lên đến 4) năm có mối tương quan mạnh (r = 0-87) với sự mở rộng của các tế bào CD8+. Qua phân tích bằng MoAbs, không có ưu thế nào đối với việc sử dụng các gia đình gen TCR-Vβ cụ thể vào bất kỳ thời điểm nào trong nhiễm CMV nguyên phát. Do đó, sự tồn tại của tình trạng lymphocyt CD8 là mối liên hệ trực tiếp với tỷ lệ mở rộng của một phân nhóm CD8+ CD57- không phổ biến và sự thay thế tiến triển của nó bằng các tế bào T CD8+ CD57+ được kích thích mạn tính bởi CMV.\u003C\u002Fjats:p>",{"EN":1310,"VI":1311},"CD8 lymphocytosis in primary cytomegalovirus (CMV) infection of allograft recipients: expansion of an uncommon CD8+ CD57− subset and its progressive replacement by CD8+CD57+ T cells","Tăng sinh CD8 lymphocyt trong nhiễm virus cytomegalovirus (CMV) nguyên phát ở người nhận ghép tạng: sự mở rộng của một phân nhóm CD8+ CD57− không phổ biến và sự thay thế tiến triển của nó bằng các tế bào T CD8+CD57+",{"VOID":1313},"7511079",{"VOID":1315},"10.1111\u002Fj.1365-2249.1994.tb07020.x",[186],[1318],"VI","https:\u002F\u002Facademic.oup.com\u002Fcei\u002Farticle\u002F95\u002F3\u002F465\u002F6490871",[1321,1340,1355,1372,1389],{"id":1322,"sortIndex":25,"researcher":24,"roles":1323,"affiliations":1324,"properties":1333,"displayName":1337,"givenName":24,"familyName":24},"37ba7433-cc5e-48c2-b0fd-044e598cc188",[],[1325],{"id":1326,"sortIndex":25,"affiliation":1327,"properties":24},"c448f7aa-6000-4036-82e1-0e8b7186225d",{"id":1326,"createTime":24,"updateTime":24,"relativeEntities":1328,"slug":24,"properties":1329,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1332,"statistic":24},[],{"title":1330},{"EN":1331},"Service d'Immunologie Faculté de Médecine, Centre Hospitalier et Universitaire de Lille, Lille, France",[],{"orcid":1334,"title":1336,"openalex":1338},{"VOID":1335},"https:\u002F\u002Forcid.org\u002F0000-0002-1524-9891",{"EN":1337},"Myriam Labalette",{"VOID":1339},"A5041359686",{"id":1341,"sortIndex":104,"researcher":24,"roles":1342,"affiliations":1343,"properties":1350,"displayName":1352,"givenName":24,"familyName":24},"2e97c37b-1734-4d8e-8ed8-654ca030f0a6",[],[1344],{"id":1326,"sortIndex":25,"affiliation":1345,"properties":24},{"id":1326,"createTime":24,"updateTime":24,"relativeEntities":1346,"slug":24,"properties":1347,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1349,"statistic":24},[],{"title":1348},{"EN":1331},[],{"title":1351,"openalex":1353},{"EN":1352},"F. 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1989, Peripheral T lymphocytes: expansion potential and homeostatic regulation of pool sizes and CD4\u002FCD8 ratios in vivo, Eur J Immunol, 19, 905, 10.1002\u002Feji.1830190518",{"doi":1468},"10.1002\u002Feji.1830190518",{"id":24,"text":1470,"url":24,"identifiers":1471},"Borysiewicz, 1988, Human cytomegalovirus-specific cytotoxic T cells: their precursor frequency and stage specificity, Eur J Immunol, 18, 269, 10.1002\u002Feji.1830180214",{"doi":1472},"10.1002\u002Feji.1830180214",{"id":24,"text":1474,"url":24,"identifiers":1475},"Reusser, 1991, Cytotoxic Tlymphocyte response to cytomegalovirus after human allogeneic bone marrow transplantation: pattern of recovery and correlation with cytomegalovirus infection and disease, Blood, 78, 1373, 10.1182\u002Fblood.V78.5.1373.1373",{"doi":1476},"10.1182\u002Fblood.V78.5.1373.1373",{"id":24,"text":1478,"url":24,"identifiers":1479},"Carney, 1981, Analysis of T lymphocyte subsets in cytomegalovirus mononucleosis, J Immunol, 126, 2114, 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10.1016\u002F0192-0561(81)90024-2",{"doi":1494},"10.1016\u002F0192-0561(81)90024-2",{"id":24,"text":1496,"url":24,"identifiers":1497},"Maher, 1985, Cytomegalovirus infection in cardiac transplant recipients associated with chronic T cell subset ratio inversion with expansion of a Leu-7+ Ts-e+ subset, Clin Exp Immunol, 62, 515",{},{"id":24,"text":1499,"url":24,"identifiers":1500},"Yumada, 1985, Monoclonal antibody 9.3 and anti-CDll antibodies define reciprocal subsets of lymphocytes, Eur J Immunol, 15, 1164, 10.1002\u002Feji.1830151204",{"doi":1501},"10.1002\u002Feji.1830151204",{"id":24,"text":1503,"url":24,"identifiers":1504},"Gratama, 1988, Flow eytometric and morphologic studies of HNKl+ (Leu-7+) lymphocytes in relation to cytomegalovirus carrier status, Clin Exp Immunol, 74, 190",{},{"id":24,"text":1506,"url":24,"identifiers":1507},"Gratama, 1989, Phenotypic study of CD4+ and CD8+ lymphocyte subsets in relation to cytomegalovirus carrier status and its correlate with pokeweed mitogen-indueed B lymphocyte differentiation, Clin Exp Immunol, 77, 245",{},{"id":24,"text":1509,"url":24,"identifiers":1510},"Forman, 1985, Increased Leu-7-positive T lymphocytes during cytomegalovirus infection following allogeneie bone marrow transplantation for hematologic malignancies, Transplantation, 41, 268",{},{"id":24,"text":1512,"url":24,"identifiers":1513},"Würsch, 1985, The effect of cytomegalovirus infection on T lymphocytes after allogeneic bone marrow transplantation, Clin Exp Immunol, 62, 278",{},{"id":24,"text":1515,"url":24,"identifiers":1516},"Renzi, 1987, Analysis of T cell subsets in normal adults. Comparison of whole blood lysis technique to Ficol-Hypaque separation by flow cytometry, J Immunol Methods, 98, 53, 10.1016\u002F0022-1759(87)90434-0",{"doi":1517},"10.1016\u002F0022-1759(87)90434-0",{"id":24,"text":1519,"url":24,"identifiers":1520},"Rees, 1989, Changes in lymphocyte subset distribution aid in the differential diagnosis of renal allograft dysfunction, J Clin Lab Anal, 3, 222, 10.1002\u002Fjcla.1860030406",{"doi":1521},"10.1002\u002Fjcla.1860030406",{"id":24,"text":1523,"url":24,"identifiers":1524},"Siegel, 1989, Discriminating rejection from CMV infection in renal allograft recipients using How cytometry, Clin Immunol Immunopathol, 51, 157, 10.1016\u002F0090-1229(89)90016-0",{"doi":1525},"10.1016\u002F0090-1229(89)90016-0",{"id":24,"text":1527,"url":24,"identifiers":1528},"Fujimoto, 1983, Spontaneous release of Leu-2 (T8) molecule from human T cells, J Exp Med, 159, 752, 10.1084\u002Fjem.158.3.752",{"doi":1529},"10.1084\u002Fjem.158.3.752",{"id":24,"text":1531,"url":24,"identifiers":1532},"Reddy, 1989, Elevated soluble CD8 levels in sera of human immunodeficiency virus-infected populations, J Clin Microbiol, 27, 257, 10.1128\u002Fjcm.27.2.257-260.1989",{"doi":1533},"10.1128\u002Fjcm.27.2.257-260.1989",{"id":24,"text":1535,"url":24,"identifiers":1536},"Meyers, 1990, Cytomegalovirus excretion as a predictor of cytomegalovirus disease after marrow transplantation: importance of cytomegalovirus viremia, J Infect Dis, 162, 373, 10.1093\u002Finfdis\u002F162.2.373",{"doi":1537},"10.1093\u002Finfdis\u002F162.2.373",{"id":24,"text":1539,"url":24,"identifiers":1540},"Van Den Berg, 1992, Recovery from cytomegalovirus infection is associated with activation of peripheral blood lymphocytes, J Infect Dis, 166, 1228, 10.1093\u002Finfdis\u002F166.6.1228",{"doi":1541},"10.1093\u002Finfdis\u002F166.6.1228",{"id":24,"text":1543,"url":24,"identifiers":1544},"Van Den Berg, 1993, Prediction of recurrent cytomegalovirus disease after treatment with ganeiclovir in solid-organ transplant recipients, Transplantation, 55, 847, 10.1097\u002F00007890-199304000-00031",{"doi":1545},"10.1097\u002F00007890-199304000-00031",{"id":24,"text":1547,"url":24,"identifiers":1548},"Tilden, 1983, Suppressor cell function of human granular lymphocytes identified by the HNK-I (Leu-7) monoclonal antibody, J Immunol, 130, 1171, 10.4049\u002Fjimmunol.130.3.1171",{"doi":1549},"10.4049\u002Fjimmunol.130.3.1171",{"id":24,"text":1551,"url":24,"identifiers":1552},"Divine, 1988, Functional analysis of CD8 lymphocytes in long-term surviving patients after bone marrow transplantation, J Clin Immunol, 8, 140, 10.1007\u002FBF00917902",{"doi":1553},"10.1007\u002FBF00917902",{"id":24,"text":1555,"url":24,"identifiers":1556},"Sadal-Sowti, 1991, A lectin-binding soluble factor released by CD8+ CD57+ lymphoeytes from AIDS patients inhibits T cell cytotoxicity, Eur J Immunol, 21, 737, 10.1002\u002Feji.1830210329",{"doi":1557},"10.1002\u002Feji.1830210329",{"id":24,"text":1559,"url":24,"identifiers":1560},"McFarland, 1992, CDIlb (Mac-1): a marker for CD8+ cytotoxic T cell activation and memory in virus infection, J Immunol, 149, 1326, 10.4049\u002Fjimmunol.149.4.1326",{"doi":1561},"10.4049\u002Fjimmunol.149.4.1326",{"id":24,"text":1563,"url":24,"identifiers":1564},"Linsley, 1993, CD28 engagement by B7\u002FBB-I induces transient down-regulation of CD28 synthesis and prolonged unresponsiveness to CD28 signaling, J Immunol, 150, 3161, 10.4049\u002Fjimmunol.150.8.3161",{"doi":1565},"10.4049\u002Fjimmunol.150.8.3161",{"id":24,"text":1567,"url":24,"identifiers":1568},"Azuma, 1993, CD28- T lymphocytes. Antigenic and functional properties, J Immunol, 150, 1147, 10.4049\u002Fjimmunol.150.4.1147",{"doi":1569},"10.4049\u002Fjimmunol.150.4.1147",{"id":24,"text":1571,"url":24,"identifiers":1572},"Kruse, 1984, Neural cell adhesion molecules and myetin-associated glycoprotein share a common carbohydrate moiety recognized by monoclonal antibodies L2 and HNK-1, Nature, 311, 153, 10.1038\u002F311153a0",{"doi":1573},"10.1038\u002F311153a0",{"id":24,"text":1575,"url":24,"identifiers":1576},"Reipert, 1992, CD3+ CD57+ lymphocytes are not likely to be involved in antigen-specific rejection processes in long-term allograft recipients, Clin Exp Immunol, 89, 143, 10.1111\u002Fj.1365-2249.1992.tb06893.x",{"doi":1577},"10.1111\u002Fj.1365-2249.1992.tb06893.x",{"id":1579,"createTime":1580,"updateTime":1580,"relativeEntities":1581,"slug":1582,"properties":1583,"entityType":182,"verifyStatus":183,"verifyTime":1580,"verifyNote":184,"languages":1598,"translateLanguages":24,"viewCount":25,"primaryUrl":1599,"fullTextUrl":24,"authors":1600,"publicationType":389,"publisherRelationship":1667,"citationCount":1721,"citationInfo":1722,"publishDate":1725,"publishYear":1723,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1726,"openAccess":24,"references":1727,"isForceReanalyzing":570},"c7c892cf-bd56-433f-8954-f2ff81e8aeef","2025-02-10T18:43:16.748+00:00",[],"Increased-levels-of-IL-13-mRNA-but-not-IL-4-mRNA-are-found-i-in-vivo-i-in-peripheral-blood-mononuclear-cells-PBMC-of-patients-with-atopic-dermatitis-AD-",{"mag":1584,"pmc":1586,"openalex":1588,"abstract":1590,"title":1592,"pm":1594,"doi":1596},{"VOID":1585},"2035820019",{"VOID":1587},"1904670",{"VOID":1589},"W2035820019",{"EN":1591},"\u003Cjats:title>SUMMARY\u003C\u002Fjats:title>\n               \u003Cjats:p>Previous studies using in vitro systems with various stimuli have shown that PBMC from patients with AD show increased levels of IL-4 but decreased levels of interferon-gamma (IFN-γ) compared with PBMC from normal controls. However, in vitro conditions do not always mimic the in vivo condition. We therefore believe that it is important to quantify the expression of these cytokines in freshly isolated PBMC. This study examines the expression of IFN-γ, IL-4 and IL-13 mRNA in freshly isolated PBMC from adult patients with AD, from patients with psoriasis vulgaris and from healthy adults, using the semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method. Levels of IFN-γ mRNA were significantly lower in PBMC of patients with AD than in controls. IL-4 mRNA levels did not differ significantly between groups. Conversely, levels of mRNA for IL-13 were significantly greater in PBMC of patients with AD than in controls. An increase in IL-13 expression may regulate the in vivo synthesis of IgE in patients with AD.\u003C\u002Fjats:p>",{"EN":1593},"Increased levels of IL-13 mRNA, but not IL-4 mRNA, are found \u003Ci>in vivo\u003C\u002Fi> in peripheral blood mononuclear cells (PBMC) of patients with atopic dermatitis 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helper type 9 (Th9) cells are a novel identified subset of CD4+ T helper cells, which could partly contribute to allergic inflammation, while the precise contribution of Th9 cells in atopic dermatitis (AD) remains unknown. We aimed to explore the possible role of Th9 cells in AD pathogenesis. The Th9 cell percentage, transcription factor PU.1 and cytokine interleukin (IL)-9 mRNA levels, as well as IL-9 serum concentration in peripheral circulation, were measured in AD patients, psoriasis patients and healthy controls. The Th9 cell percentage, PU.1 and IL-9 expression levels of AD patients were all increased significantly compared with the other two control groups (P < 0·01), and correlated positively with SCORing Atopic Dermatitis index, serum immunoglobulin (Ig)E and thymus- and activation-regulated chemokine (TARC) levels (P < 0·05). In simple AD patients and AD patients complicated by allergic rhinitis or asthma, there were no significant differences in the Th9 cell percentage, PU.1 and IL-9 expression levels between them. At the same time, IL-9 and vascular endothelial growth factor (VEGF) mRNA levels were detected in AD lesions and normal skin samples, which were both distinctly elevated in AD lesions, and there was a positive association between them (P < 0·01). Keratinocytes were cultured with IL-9 stimulation and the secretion of VEGF was detected. IL-9 can promote the secretion of VEGF by keratinocytes in a time- and dose-dependent manner. 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are associated with clinical severity in children with atopic dermatitis, Pediatr Dermatol, 30, 222, 10.1111\u002Fj.1525-1470.2012.01766.x",{"doi":1991},"10.1111\u002Fj.1525-1470.2012.01766.x",{"id":24,"text":1993,"url":24,"identifiers":1994},"van Leeuwen, 1989, Molecular organization of the cytokine gene cluster, involving the human IL-3, IL-4, IL-5, and GM-CSF genes, on human chromosome 5, Blood, 73, 1142, 10.1182\u002Fblood.V73.5.1142.1142",{"doi":1995},"10.1182\u002Fblood.V73.5.1142.1142",{"id":24,"text":1997,"url":24,"identifiers":1998},"Postma, 1995, Genetic susceptibility to asthma – bronchial hyperresponsiveness coinherited with a major gene for atopy, N Engl J Med, 333, 894, 10.1056\u002FNEJM199510053331402",{"doi":1999},"10.1056\u002FNEJM199510053331402",{"id":24,"text":2001,"url":24,"identifiers":2002},"Noguchi, 1997, Evidence for linkage between asthma\u002Fatopy in childhood and chromosome 5q31-q33 in a Japanese population, Am J Respir Crit Care Med, 156, 1390, 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imbalance of interferon-gamma (IFN-γ)-bearing CD4+ T (Th1) cells in the pathogenesis of AD is well recognized; however, a possible role in AD for CD8+ T cells secreting Th1-like cytokines (Tc1) has not been properly addressed. In this study, two- and three-colour FACS analysis allowed us to discriminate the Th1 from the Tc1 subset. AD patients had half the number of IFN-γ-producing circulating T cells (P < 0.005; 13.6 ± 1.9% (mean ± s.d.)) compared with normal donors (25.0 ± 2.4%). Specifically, both Th1 (4.8 ± 0.7%) and Tc1 (8.1 ± 1.1%) cells in AD were decreased compared with Th1 (8.8 ± 0.8%) and Tc1 (15.0 ± 1.5%) cells in controls. Moreover, at the mRNA level, the ratios of IFN-γ\u002FIL-4 and IFN-γ\u002FIL-10 were lower in cells from AD patients compared with controls. In conclusion, the decrease of IFN-γ-producing T lymphocytes in AD is due to a reduction in both Th1 and Tc1 IFN-γ-secreting cells; this may not only contribute to the over-production of IgE, but also explain the high incidence of cutaneous infections observed in AD patients.\u003C\u002Fjats:p>",{"EN":2054},"Reduced production of both Th1 and Tc1 lymphocyte subsets in atopic dermatitis 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Atopic dermatitis. In: Fitzpatrick TB, Eisen AZ, Wolff Ket al., eds. Dermatology in general medicine. New York: McGraw-Hill, 1993 :1543, 64 .",{},{"id":24,"text":2355,"url":24,"identifiers":2356},"Sanders B, 1991, Immunol Rev, 119, 65, 10.1111\u002Fj.1600-065X.1991.tb00578.x",{"doi":2357},"10.1111\u002Fj.1600-065X.1991.tb00578.x",{"id":24,"text":2359,"url":24,"identifiers":2360},"10.1016\u002F0022-1759(93)90158-4",{"doi":2359},{"id":24,"text":2362,"url":24,"identifiers":2363},"Borthwich NJ, 1994, AIDS, 8, 431, 10.1097\u002F00002030-199404000-00004",{"doi":904},{"id":24,"text":2365,"url":24,"identifiers":2366},"Graziosi C, 1994, Science, 265, 248, 10.1126\u002Fscience.8023143",{"doi":2367},"10.1126\u002Fscience.8023143",{"id":24,"text":2369,"url":24,"identifiers":2370},"Yamamura M, 1992, J Immunol, 149, 1470, 10.4049\u002Fjimmunol.149.4.1470",{"doi":2371},"10.4049\u002Fjimmunol.149.4.1470",{"id":24,"text":2373,"url":24,"identifiers":2374},"10.1016\u002F0167-5699(94)90152-X",{"doi":2373},{"id":24,"text":2376,"url":24,"identifiers":2377},"Fong TAT, 1990, J Immunol, 144, 1744, 10.4049\u002Fjimmunol.144.5.1744",{"doi":2378},"10.4049\u002Fjimmunol.144.5.1744",{"id":24,"text":2380,"url":24,"identifiers":2381},"Croft M, 1994, J Exp Med, 180, 1715, 10.1084\u002Fjem.180.5.1715",{"doi":2382},"10.1084\u002Fjem.180.5.1715",{"id":24,"text":2384,"url":24,"identifiers":2385},"Carter LL, 1995, J Immunol, 155, 1028, 10.4049\u002Fjimmunol.155.3.1028",{"doi":2386},"10.4049\u002Fjimmunol.155.3.1028",{"id":24,"text":2388,"url":24,"identifiers":2389},"Lacour M, 1993, Clin Rev Allergy, 11, 491",{},{"id":24,"text":2391,"url":24,"identifiers":2392},"10.1016\u002F1074-7613(95)90051-9",{"doi":2391},{"id":24,"text":2394,"url":24,"identifiers":2395},"Cronin DC, 1995, J Immunol, 154, 3118, 10.4049\u002Fjimmunol.154.7.3118",{"doi":2396},"10.4049\u002Fjimmunol.154.7.3118",{"id":24,"text":2398,"url":24,"identifiers":2399},"Seder RA, 1995, J Exp Med, 181, 5, 10.1084\u002Fjem.181.1.5",{"doi":2400},"10.1084\u002Fjem.181.1.5",{"id":2402,"createTime":2403,"updateTime":2403,"relativeEntities":2404,"slug":2405,"properties":2406,"entityType":182,"verifyStatus":183,"verifyTime":2421,"verifyNote":184,"languages":2422,"translateLanguages":24,"viewCount":25,"primaryUrl":2423,"fullTextUrl":24,"authors":2424,"publicationType":389,"publisherRelationship":2506,"citationCount":2560,"citationInfo":2561,"publishDate":2563,"publishYear":772,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2564,"openAccess":24,"references":2565,"isForceReanalyzing":570},"f649171f-59a5-4483-a3a7-7b3eb0dd9135","2025-02-10T15:50:10.750+00:00",[],"CD4-and-CD8-clonal-T-cell-expansions-indicate-a-role-of-antigens-inankylosing-spondylitis-a-study-in-HLA-B27-monozygotic-twins",{"mag":2407,"pmc":2409,"openalex":2411,"abstract":2413,"title":2415,"pm":2417,"doi":2419},{"VOID":2408},"2073498606",{"VOID":2410},"1905979",{"VOID":2412},"W2073498606",{"EN":2414},"\u003Cjats:title>SUMMARY\u003C\u002Fjats:title>\u003Cjats:p>Ankylosing spondylitis (AS) is a complex genetic disease in which both MHC and non-MHC genes determine disease susceptibility. To determine whether the T cell repertoires of individuals with AS show signs of increased stimulation by exogenous antigens, CD4+ and CD8+ T cell subsets of five monozygotic HLA-B27+ twins (two concordant and three discordant for AS) and CD8+ T cell repertoires of three healthy HLA-B27+ individuals were characterized by TCR β-chain (TCRB) CDR3 size spectratyping. Selected TCRB-CDR3 spectra were further analysed by BJ-segment analysis and TCRB-CDR3 from expanded T cell clones were sequenced. In an analysis of all data (519\u002F598 possible TCRB-CDR3 spectra), AS was associated with increased T cell oligoclonality in both CD8+ (P = 0·0001) and CD4+ (P = 0·033) T cell subsets. This was also evident when data were compared between individual twins. Nucleotide sequence analysis of expanded CD8+ or CD4+ T cell clones did not show selection for particular TCRB-CDR3 amino acid sequence motifs but displayed sequence homologies with published sequences from intra-epithelial lymphocytes or synovial T cells from rheumatoid arthritis patients. Together, these results provide support for the hypothesis that responses to T cell-stimulating exogenous or endogenous antigens are involved in the induction and\u002For maintenance of AS.\u003C\u002Fjats:p>",{"EN":2416},"CD4+ and CD8+ clonal T cell expansions indicate a role of antigens inankylosing spondylitis; a study in HLA-B27+ monozygotic twins",{"VOID":2418},"11207664",{"VOID":2420},"10.1046\u002Fj.1365-2249.2001.01440.x","2025-02-10T15:50:10.749+00:00",[186],"https:\u002F\u002Facademic.oup.com\u002Fcei\u002Farticle\u002F123\u002F2\u002F315\u002F6461477",[2425,2442,2459,2474,2489],{"id":2426,"sortIndex":25,"researcher":24,"roles":2427,"affiliations":2428,"properties":2437,"displayName":2439,"givenName":24,"familyName":24},"f63f4728-6b9f-462c-838a-396aa7455dc3",[],[2429],{"id":2430,"sortIndex":25,"affiliation":2431,"properties":24},"9b04406d-cb1d-4489-a316-5552bca94e2c",{"id":2430,"createTime":24,"updateTime":24,"relativeEntities":2432,"slug":24,"properties":2433,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2436,"statistic":24},[],{"title":2434},{"EN":2435},"Internal Medicine II, University of the Saarland, Hamberg and",[],{"title":2438,"openalex":2440},{"EN":2439},"Rainer Duchmann",{"VOID":2441},"A5051790206",{"id":2443,"sortIndex":104,"researcher":24,"roles":2444,"affiliations":2445,"properties":2454,"displayName":2456,"givenName":24,"familyName":24},"3847afaa-e5f0-4b7f-8317-954355c5f6bc",[],[2446],{"id":2447,"sortIndex":25,"affiliation":2448,"properties":24},"09d14bf5-fde6-4e45-9976-6619bfc983e6",{"id":2447,"createTime":24,"updateTime":24,"relativeEntities":2449,"slug":24,"properties":2450,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2453,"statistic":24},[],{"title":2451},{"EN":2452},"Department of Medicine, Johannes Gutenberg University of Mainz, Mainz, Germany",[],{"title":2455,"openalex":2457},{"EN":2456},"Carsten Lambert",{"VOID":2458},"A5014850676",{"id":2460,"sortIndex":114,"researcher":24,"roles":2461,"affiliations":2462,"properties":2469,"displayName":2471,"givenName":24,"familyName":24},"d936f697-fe42-4b28-b323-5853f47ebbaa",[],[2463],{"id":2447,"sortIndex":25,"affiliation":2464,"properties":24},{"id":2447,"createTime":24,"updateTime":24,"relativeEntities":2465,"slug":24,"properties":2466,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2468,"statistic":24},[],{"title":2467},{"EN":2452},[],{"title":2470,"openalex":2472},{"EN":2471},"Ekkehard May",{"VOID":2473},"A5025414860",{"id":2475,"sortIndex":102,"researcher":24,"roles":2476,"affiliations":2477,"properties":2484,"displayName":2486,"givenName":24,"familyName":24},"c2ae03e7-34d3-4d7e-be2c-514708d1ed84",[],[2478],{"id":2447,"sortIndex":25,"affiliation":2479,"properties":24},{"id":2447,"createTime":24,"updateTime":24,"relativeEntities":2480,"slug":24,"properties":2481,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2483,"statistic":24},[],{"title":2482},{"EN":2452},[],{"title":2485,"openalex":2487},{"EN":2486},"Thomas Höhler",{"VOID":2488},"A5109321050",{"id":2490,"sortIndex":113,"researcher":24,"roles":2491,"affiliations":2492,"properties":2499,"displayName":2503,"givenName":24,"familyName":24},"aaaaedb0-4fb2-45b9-8a2d-f1fd29d0269c",[],[2493],{"id":2447,"sortIndex":25,"affiliation":2494,"properties":24},{"id":2447,"createTime":24,"updateTime":24,"relativeEntities":2495,"slug":24,"properties":2496,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2498,"statistic":24},[],{"title":2497},{"EN":2452},[],{"orcid":2500,"title":2502,"openalex":2504},{"VOID":2501},"https:\u002F\u002Forcid.org\u002F0000-0001-6446-6246",{"EN":2503},"E. 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chains in human intestinal mucosa, J Exp Med, 180, 1337, 10.1084\u002Fjem.180.4.1337",{"doi":2628},"10.1084\u002Fjem.180.4.1337",{"id":24,"text":2630,"url":24,"identifiers":2631},"Pluschke, 1994, Oligoclonality and skewed T cell receptor V beta gene segment expression in in vivo activated human intestinal intraepithelial T lymphocytes, Immunobiology, 192, 77, 10.1016\u002FS0171-2985(11)80409-2",{"doi":2632},"10.1016\u002FS0171-2985(11)80409-2",{"id":24,"text":2634,"url":24,"identifiers":2635},"Diu, 1993, Limited T-cell receptor diversity in liver-infiltrating lymphocytes from patients with primary biliary cirrhosis, J Autoimmun, 6, 611, 10.1006\u002Fjaut.1993.1050",{"doi":2636},"10.1006\u002Fjaut.1993.1050",{"id":24,"text":2638,"url":24,"identifiers":2639},"Howell, 1991, Limited T-cell receptor beta-chain heterogeneity among interleukin 2 receptor-positive synovial T cells suggests a role for superantigen in rheumatoid arthritis, Proc Natl Acad Sci USA, 88, 10921, 10.1073\u002Fpnas.88.23.10921",{"doi":2640},"10.1073\u002Fpnas.88.23.10921",{"id":24,"text":2642,"url":24,"identifiers":2643},"Striebich, 1998, Selective accumulation of related CD4+ T cell clones in the synovial fluid of patients with rheumatoid arthritis, J Immunol, 4428",{},{"id":24,"text":2645,"url":24,"identifiers":2646},"Zhou, 1998, The specificity of peptides bound to human histocompatibility leukocyte antigen (HLA)-B27 influences the prevalence of arthritis in HLA-B27 transgenic rats, J Exp Med, 188, 877, 10.1084\u002Fjem.188.5.877",{"doi":2647},"10.1084\u002Fjem.188.5.877",{"id":24,"text":2649,"url":24,"identifiers":2650},"Hermann, 1993, HLA-B27-restricted CD8 T cells derived form synovial fluids of patients with reactive arthritis and ankylosing spondylitis, Lancet, 342, 646, 10.1016\u002F0140-6736(93)91760-J",{"doi":2651},"10.1016\u002F0140-6736(93)91760-J",{"id":24,"text":2653,"url":24,"identifiers":2654},"Ugrinovic, 1997, A single nonamer from the Yersinia 60-kDa heat shock protein is the target of HLA-B27-restricted CTL response in Yersinia-induced reactive arthritis, J Immunol, 159, 5715, 10.4049\u002Fjimmunol.159.11.5715",{"doi":2655},"10.4049\u002Fjimmunol.159.11.5715",{"id":24,"text":2657,"url":24,"identifiers":2658},"May, 2000, Identical T cell expansions in the colon mucosa and the synovium of a patient with enterogenic spondylarthropathy, Gastroenterol",{},{"id":24,"text":2660,"url":24,"identifiers":2661},"Posnett, 1994, Clonal populations of T cells in normal elderly humans: the T cell equivalent to ‘benign monoclonal gammopathy’, J Exp Med, 179, 609, 10.1084\u002Fjem.179.2.609",{"doi":2662},"10.1084\u002Fjem.179.2.609",{"id":24,"text":2664,"url":24,"identifiers":2665},"Hingorani, 1993, Clonal predominance of T cell receptors within the CD8+ CD45RO+ subset in normal human subjects, J Immunol, 151, 5762, 10.4049\u002Fjimmunol.151.10.5762",{"doi":2666},"10.4049\u002Fjimmunol.151.10.5762",{"id":24,"text":2668,"url":24,"identifiers":2669},"Wang, 1995, CD8highCD57+ T lymphocytes in normal, healthy individuals are oligoclonal and respond to human cytomegalovirus, J Immunol, 155, 5046, 10.4049\u002Fjimmunol.155.10.5046",{"doi":2670},"10.4049\u002Fjimmunol.155.10.5046",{"id":24,"text":2672,"url":24,"identifiers":2673},"Morley, 1995, Oligoclonal CD8+ T cells are preferentially expanded in the CD57+ subset, J Immunol, 154, 6182, 10.4049\u002Fjimmunol.154.11.6182",{"doi":2674},"10.4049\u002Fjimmunol.154.11.6182",{"id":24,"text":2676,"url":24,"identifiers":2677},"Bowness, 1994, Identification of T cell receptor recognition residues for a viral peptide presented by HLA B27, Eur J Immunol, 24, 2357, 10.1002\u002Feji.1830241015",{"doi":2678},"10.1002\u002Feji.1830241015",{"id":24,"text":2680,"url":24,"identifiers":2681},"Bragado, 1990, T cell receptor V beta gene usage in a human alloreactive response. Shared structural features among HLA-B27-specific T cell clones, J Exp Med, 171, 1189, 10.1084\u002Fjem.171.4.1189",{"doi":2682},"10.1084\u002Fjem.171.4.1189",{"id":24,"text":2684,"url":24,"identifiers":2685},"Lauzurica, 1992, Asymmetric selection of T cell antigen receptor α and β chains in HLA-B27 alloreactivity, J Immunol, 3624",{},{"id":24,"text":2687,"url":24,"identifiers":2688},"Dulphy, 1999, Common intra-articular T cell expansions in patients with reactive arthritis: identical beta-chain junctional sequences and cytotoxicity toward HLA-B27, J Immunol, 162, 3830, 10.4049\u002Fjimmunol.162.7.3830",{"doi":2689},"10.4049\u002Fjimmunol.162.7.3830",{"id":24,"text":2691,"url":24,"identifiers":2692},"Alam, 1996, Persistence of dominant T cell clones in synovial tissues during rheumatoid arthritis, J Immunol, 156, 3480, 10.4049\u002Fjimmunol.156.9.3480",{"doi":2693},"10.4049\u002Fjimmunol.156.9.3480",{"id":24,"text":2695,"url":24,"identifiers":2696},"Mielants, 1986, Familial aggregation in seronegative spondylarthritis of enterogenic origin. A family study, J Rheumatol, 13, 126",{},{"id":24,"text":2698,"url":24,"identifiers":2699},"Mertz, 2000, Multispecific CD4+ T cell response to a single 12-mer epitope of the immunodominant heat-shock protein 60 of Yersinia enterocolitica in Yersinia-triggered reactive arthritis: overlap with the B27-restricted CD8 epitope, functional properties, and epitope presentation by multiple DR alleles, J Immunol, 164, 1529, 10.4049\u002Fjimmunol.164.3.1529",{"doi":2700},"10.4049\u002Fjimmunol.164.3.1529",{"id":24,"text":2702,"url":24,"identifiers":2703},"Breban, 1996, T cells, but not thymic exposure to HLA-B27, are required for the inflammatory disease of HLA-B27 transgenic rats, J Immunol, 156, 794, 10.4049\u002Fjimmunol.156.2.794",{"doi":2704},"10.4049\u002Fjimmunol.156.2.794",{"id":24,"text":2706,"url":24,"identifiers":2707},"Fiorillo, 2000, CD8(+) T-cell autoreactivity to an HLA-B27-restricted self-epitope correlates with ankylosing spondylitis, J Clin Invest, 106, 47, 10.1172\u002FJCI9295",{"doi":2708},"10.1172\u002FJCI9295",{"id":2710,"createTime":2711,"updateTime":2711,"relativeEntities":2712,"slug":2713,"properties":2714,"entityType":182,"verifyStatus":183,"verifyTime":2711,"verifyNote":184,"languages":2729,"translateLanguages":24,"viewCount":25,"primaryUrl":2730,"fullTextUrl":24,"authors":2731,"publicationType":389,"publisherRelationship":2872,"citationCount":2926,"citationInfo":2927,"publishDate":2929,"publishYear":1907,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2930,"openAccess":24,"references":2931,"isForceReanalyzing":570},"583df028-d277-4a35-886f-2ed6c8e90a00","2025-02-09T14:22:15.897+00:00",[],"Plasma-levels-of-mannan-binding-lectin-MBL-associated-serine-proteases-MASPs-and-MBL-associated-protein-in-cardio-and-cerebrovascular-diseases",{"mag":2715,"pmc":2717,"openalex":2719,"abstract":2721,"title":2723,"pm":2725,"doi":2727},{"VOID":2716},"1484854422",{"VOID":2718},"3694541",{"VOID":2720},"W1484854422",{"EN":2722},"\u003Cjats:title>Summary\u003C\u002Fjats:title>\n               \u003Cjats:p>Growing evidence suggests a prominent role of the complement system in the pathogenesis of cardio- and cerebrovascular diseases (CVD). Mannan-binding lectin-associated serine proteases (MASPs) MASP-1 and MASP-2 of the complement lectin pathway contribute to clot formation and may represent an important link between inflammation and thrombosis. MBL-associated protein MAp44 has shown cardioprotective effects in murine models. However, MAp44 has never been measured in patients with CVD and data on MASP levels in CVD are scarce. Our aim was to investigate for the first time plasma levels of MAp44 and MASP-1, -2, -3 concomitantly in patients with CVD. We performed a pilot study in 50 healthy volunteers, in stable coronary artery disease (CAD) patients with one-vessel (n = 51) or three-vessel disease (n = 53) and age-matched controls with normal coronary arteries (n = 53), 49 patients after myocardial infarction (MI) and 66 patients with acute ischaemic stroke. We measured MAp44 and MASP-1 levels by in-house time-resolved immunofluorometric assays. MASP-2 and MASP-3 levels were measured using commercial enzyme-linked immunosorbent assay kits. MASP-1 levels were highest in subacute MI patients and lowest in acute stroke patients. MASP-2 levels were lower in MI and stroke patients compared with controls and CAD patients. MASP-3 and MAp44 levels did not differ between groups. MASP or MAp44 levels were not associated with severity of disease. MASP and MAp44 levels were associated with cardiovascular risk factors including dyslipidaemia, obesity and hypertension. Our results suggest that MASP levels may be altered in vascular diseases. Larger studies are needed to confirm our results and elucidate the underlying mechanisms.\u003C\u002Fjats:p>",{"EN":2724},"Plasma levels of mannan-binding lectin (MBL)-associated serine proteases (MASPs) and MBL-associated protein in cardio- and cerebrovascular diseases",{"VOID":2726},"23607747",{"VOID":2728},"10.1111\u002Fcei.12093",[186],"https:\u002F\u002Facademic.oup.com\u002Fcei\u002Farticle\u002F173\u002F1\u002F112\u002F6420959",[2732,2749,2768,2785,2804,2821,2838,2855],{"id":2733,"sortIndex":25,"researcher":24,"roles":2734,"affiliations":2735,"properties":2744,"displayName":2746,"givenName":24,"familyName":24},"e399ca64-5ccb-4336-9c4a-e0be77f35073",[],[2736],{"id":2737,"sortIndex":25,"affiliation":2738,"properties":24},"d470fb97-1f68-46f2-8b7d-b57b47d8820c",{"id":2737,"createTime":24,"updateTime":24,"relativeEntities":2739,"slug":24,"properties":2740,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2743,"statistic":24},[],{"title":2741},{"EN":2742},"University Clinic of Haematology, Haemostasis Research Laboratory, University Hospital and University of Bern, Bern, Switzerland",[],{"title":2745,"openalex":2747},{"EN":2746},"V. 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2009, Inflammation in atherosclerosis, J Am Coll Cardiol, 54, 2129, 10.1016\u002Fj.jacc.2009.09.009",{"doi":2935},"10.1016\u002Fj.jacc.2009.09.009",{"id":24,"text":2937,"url":24,"identifiers":2938},"Carter, 2005, Inflammation, thrombosis and acute coronary syndromes, Diab Vasc Dis Res, 2, 113, 10.3132\u002Fdvdr.2005.018",{"doi":2939},"10.3132\u002Fdvdr.2005.018",{"id":24,"text":2941,"url":24,"identifiers":2942},"Oksjoki, 2007, Function and regulation of the complement system in cardiovascular diseases, Front Biosci, 12, 4696, 10.2741\u002F2419",{"doi":2943},"10.2741\u002F2419",{"id":24,"text":2945,"url":24,"identifiers":2946},"Speidl, 2011, Complement in atherosclerosis: friend or foe?, J Thromb Haemost, 9, 428, 10.1111\u002Fj.1538-7836.2010.04172.x",{"doi":2947},"10.1111\u002Fj.1538-7836.2010.04172.x",{"id":24,"text":2949,"url":24,"identifiers":2950},"Frauenknecht, 2012, Complement – a phylogenetically old system as a new player in the development of atherosclerosis [in German], Hämostaseologie, 32, 276, 10.5482\u002Fha-1191",{"doi":2951},"10.5482\u002Fha-1191",{"id":24,"text":2953,"url":24,"identifiers":2954},"Banz, 2012, Role of complement and perspectives for intervention in ischemia-reperfusion damage, Ann Med, 44, 205, 10.3109\u002F07853890.2010.535556",{"doi":2955},"10.3109\u002F07853890.2010.535556",{"id":24,"text":2957,"url":24,"identifiers":2958},"Markiewski, 2007, Complement and coagulation: strangers or partners in crime?, Trends Immunol, 28, 184, 10.1016\u002Fj.it.2007.02.006",{"doi":2959},"10.1016\u002Fj.it.2007.02.006",{"id":24,"text":2961,"url":24,"identifiers":2962},"Amara, 2010, Molecular intercommunication between the complement and coagulation systems, J Immunol, 185, 5628, 10.4049\u002Fjimmunol.0903678",{"doi":2963},"10.4049\u002Fjimmunol.0903678",{"id":24,"text":2965,"url":24,"identifiers":2966},"Ricklin, 2010, Complement: a key system for immune surveillance and homeostasis, Nat Immunol, 11, 785, 10.1038\u002Fni.1923",{"doi":2967},"10.1038\u002Fni.1923",{"id":24,"text":2969,"url":24,"identifiers":2970},"Hansen, 2010, Collectin 11 (CL-11, CL-K1) is a MASP-1\u002F3-associated plasma collectin with microbial-binding activity, J Immunol, 185, 6096, 10.4049\u002Fjimmunol.1002185",{"doi":2971},"10.4049\u002Fjimmunol.1002185",{"id":24,"text":2973,"url":24,"identifiers":2974},"Yongqing, 2012, Mannose-binding lectin serine proteases and associated proteins of the lectin pathway of complement: two genes, five proteins and many functions?, Biochim Biophys Acta, 1824, 253, 10.1016\u002Fj.bbapap.2011.05.021",{"doi":2975},"10.1016\u002Fj.bbapap.2011.05.021",{"id":24,"text":2977,"url":24,"identifiers":2978},"Degn, 2011, Disease-causing mutations in genes of the complement system, Am J Hum Genet, 88, 689, 10.1016\u002Fj.ajhg.2011.05.011",{"doi":2979},"10.1016\u002Fj.ajhg.2011.05.011",{"id":24,"text":2981,"url":24,"identifiers":2982},"Kidmose, 2012, Structural basis for activation of the 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10.1016\u002FS1074-7613(01)00161-3",{"doi":3007},"10.1016\u002FS1074-7613(01)00161-3",{"id":24,"text":3009,"url":24,"identifiers":3010},"Iwaki, 2011, The role of mannose-binding lectin-associated serine protease-3 in activation of the alternative complement pathway, J Immunol, 187, 3751, 10.4049\u002Fjimmunol.1100280",{"doi":3011},"10.4049\u002Fjimmunol.1100280",{"id":24,"text":3013,"url":24,"identifiers":3014},"Degn, 2009, MAp44, a human protein associated with pattern recognition molecules of the complement system and regulating the lectin pathway of complement activation, J Immunol, 183, 7371, 10.4049\u002Fjimmunol.0902388",{"doi":3015},"10.4049\u002Fjimmunol.0902388",{"id":24,"text":3017,"url":24,"identifiers":3018},"Skjoedt, 2012, Crystal structure and functional characterization of the complement regulator mannose-binding lectin (MBL)\u002Fficolin-associated protein-1 (MAP-1), J Biol Chem, 287, 32913, 10.1074\u002Fjbc.M112.386680",{"doi":3019},"10.1074\u002Fjbc.M112.386680",{"id":24,"text":3021,"url":24,"identifiers":3022},"Pavlov, 2012, Endogenous and natural complement inhibitor attenuates myocardial injury and arterial thrombogenesis, Circulation, 126, 2227, 10.1161\u002FCIRCULATIONAHA.112.123968",{"doi":3023},"10.1161\u002FCIRCULATIONAHA.112.123968",{"id":24,"text":3025,"url":24,"identifiers":3026},"Hajela, 2002, The biological functions of MBL-associated serine proteases (MASPs), Immunobiology, 205, 467, 10.1078\u002F0171-2985-00147",{"doi":3027},"10.1078\u002F0171-2985-00147",{"id":24,"text":3029,"url":24,"identifiers":3030},"Krarup, 2007, Simultaneous activation of complement and coagulation by MBL-associated serine protease 2, PLoS ONE, 2, e623, 10.1371\u002Fjournal.pone.0000623",{"doi":3031},"10.1371\u002Fjournal.pone.0000623",{"id":24,"text":3033,"url":24,"identifiers":3034},"Krarup, 2008, The action of MBL-associated serine protease 1 (MASP1) on factor XIII and fibrinogen, Biochim Biophys Acta, 1784, 1294, 10.1016\u002Fj.bbapap.2008.03.020",{"doi":3035},"10.1016\u002Fj.bbapap.2008.03.020",{"id":24,"text":3037,"url":24,"identifiers":3038},"Gulla, 2010, Activation of mannan-binding lectin-associated serine proteases leads to generation of a fibrin clot, Immunology, 129, 482, 10.1111\u002Fj.1365-2567.2009.03200.x",{"doi":3039},"10.1111\u002Fj.1365-2567.2009.03200.x",{"id":24,"text":3041,"url":24,"identifiers":3042},"Hess, 2012, Effects of MASP-1 of the complement system on activation of coagulation factors and plasma clot formation, PLoS ONE, 7, e35690, 10.1371\u002Fjournal.pone.0035690",{"doi":3043},"10.1371\u002Fjournal.pone.0035690",{"id":24,"text":3045,"url":24,"identifiers":3046},"La Bonte, 2012, Mannose-binding lectin-associated serine protease-1 is a significant contributor to coagulation in a murine model of occlusive thrombosis, J Immunol, 188, 885, 10.4049\u002Fjimmunol.1102916",{"doi":3047},"10.4049\u002Fjimmunol.1102916",{"id":24,"text":3049,"url":24,"identifiers":3050},"Trendelenburg, 2010, Influence of functional deficiency of complement mannose-binding lectin on outcome of patients with acute ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention, Eur Heart J, 31, 1181, 10.1093\u002Feurheartj\u002Fehp597",{"doi":3051},"10.1093\u002Feurheartj\u002Fehp597",{"id":24,"text":3053,"url":24,"identifiers":3054},"Osthoff, 2011, Mannose-binding lectin deficiency is associated with smaller infarction size and favorable outcome in ischemic stroke patients, PLoS ONE, 6, e21338, 10.1371\u002Fjournal.pone.0021338",{"doi":3055},"10.1371\u002Fjournal.pone.0021338",{"id":24,"text":3057,"url":24,"identifiers":3058},"Mellbin, 2012, Complement activation and prognosis in patients with type 2 diabetes and myocardical infarction, Diabetes Care, 35, 911, 10.2337\u002Fdc11-1642",{"doi":3059},"10.2337\u002Fdc11-1642",{"id":24,"text":3061,"url":24,"identifiers":3062},"Zhang, 2011, MASP-2 activation is involved in ischemia-related necrotic myocardial injury, Int J Cardiol, 10.1016\u002Fj.ijcard.2011.11.032",{"doi":3063},"10.1016\u002Fj.ijcard.2011.11.032",{"id":24,"text":3065,"url":24,"identifiers":3066},"Cervera, 2010, Genetically-defined deficiency of mannose-binding lectin is associated with protection after experimental stroke in mice and outcome in human stroke, PLoS ONE, 5, e8433, 10.1371\u002Fjournal.pone.0008433",{"doi":3067},"10.1371\u002Fjournal.pone.0008433",{"id":24,"text":3069,"url":24,"identifiers":3070},"Schroeder, 2002, Thrombin activatable fibrinolysis inhibitor (TAFI) levels in patients with coronary artery disease investigated by angiography, Thromb Haemost, 88, 1020, 10.1055\u002Fs-0037-1613349",{"doi":3071},"10.1055\u002Fs-0037-1613349",{"id":24,"text":3073,"url":24,"identifiers":3074},"Schroeder, 2010, Coagulation factor XIII activation peptide and subunit levels in patients with acute ischemic stroke: a pilot study, Thromb Res, 126, e122, 10.1016\u002Fj.thromres.2010.05.027",{"doi":3075},"10.1016\u002Fj.thromres.2010.05.027",{"id":24,"text":3077,"url":24,"identifiers":3078},"Brott, 1989, Measurements of acute cerebral infarction: a clinical examination scale, Stroke, 20, 864, 10.1161\u002F01.STR.20.7.864",{"doi":3079},"10.1161\u002F01.STR.20.7.864",{"id":24,"text":3081,"url":24,"identifiers":3082},"Adams, 1993, Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in acute stroke treatment, Stroke, 24, 35, 10.1161\u002F01.STR.24.1.35",{"doi":3083},"10.1161\u002F01.STR.24.1.35",{"id":24,"text":3085,"url":24,"identifiers":3086},"Degn, 2010, Biological variations of MASP-3 and MAp44, two splice products of the MASP1 gene involved in regulation of the complement system, J Immunol Methods, 361, 37, 10.1016\u002Fj.jim.2010.07.006",{"doi":3087},"10.1016\u002Fj.jim.2010.07.006",{"id":24,"text":3089,"url":24,"identifiers":3090},"Thiel, 2012, Mannan-binding lectin (MBL)-associated serine protease-1 (MASP-1), a serine protease associated with humoral pattern-recognition molecules: normal and acute-phase levels in serum and stoichiometry of lectin pathway components, Clin Exp Immunol, 169, 38, 10.1111\u002Fj.1365-2249.2012.04584.x",{"doi":3091},"10.1111\u002Fj.1365-2249.2012.04584.x",{"id":24,"text":3093,"url":24,"identifiers":3094},"Schwaeble, 2011, Targeting of mannan-binding lectin-associated serine protease-2 confers protection from myocardial and gastrointestinal ischemia\u002Freperfusion injury, Proc Natl Acad Sci USA, 108, 7523, 10.1073\u002Fpnas.1101748108",{"doi":3095},"10.1073\u002Fpnas.1101748108",{"id":24,"text":3097,"url":24,"identifiers":3098},"Orsini, 2012, Targeting mannose-binding lectin confers long-lasting protection with a surprisingly wide therapeutic window in cerebral ischemia, Circulation, 126, 1484, 10.1161\u002FCIRCULATIONAHA.112.103051",{"doi":3099},"10.1161\u002FCIRCULATIONAHA.112.103051",{"id":24,"text":3101,"url":24,"identifiers":3102},"Møller-Kristensen, 2003, Levels of mannan-binding lectin-associated serine protease-2 in healthy individuals, J Immunol Methods, 282, 159, 10.1016\u002Fj.jim.2003.08.012",{"doi":3103},"10.1016\u002Fj.jim.2003.08.012",{"id":24,"text":3105,"url":24,"identifiers":3106},"Ytting, 2007, Biological variation in circulating levels of mannan-binding lectin (MBL) and MBL-associated serine protease-2 and the influence of age, gender and physical exercise, Scand J Immunol, 66, 458, 10.1111\u002Fj.1365-3083.2007.01991.x",{"doi":3107},"10.1111\u002Fj.1365-3083.2007.01991.x",{"id":24,"text":3109,"url":24,"identifiers":3110},"Kohler, 2002, Insulin resistance syndrome: interaction with coagulation and fibrinolysis, Swiss Med Wkly, 132, 241",{},{"id":24,"text":3112,"url":24,"identifiers":3113},"Cortesio, 2006, Mannan-binding lectin-associated serine protease 3 cleaves synthetic peptides and insulin-like growth factor-binding protein 5, Arch Biochem Biophys, 449, 164, 10.1016\u002Fj.abb.2006.02.006",{"doi":3114},"10.1016\u002Fj.abb.2006.02.006",{"id":24,"text":3116,"url":24,"identifiers":3117},"Fischer, 2004, Associations of insulin-like growth factors, insulin-like growth factor binding proteins and acid-labile subunit with coronary heart disease, Clin Endocrinol (Oxf), 61, 595, 10.1111\u002Fj.1365-2265.2004.02136.x",{"doi":3118},"10.1111\u002Fj.1365-2265.2004.02136.x",{"id":24,"text":3120,"url":24,"identifiers":3121},"Conti, 2011, IGF-1 and atherothrombosis: relevance to pathophysiology and therapy, Clin Sci, 120, 377, 10.1042\u002FCS20100400",{"doi":3122},"10.1042\u002FCS20100400",{"id":3124,"createTime":3125,"updateTime":3125,"relativeEntities":3126,"slug":3127,"properties":3128,"entityType":182,"verifyStatus":183,"verifyTime":3125,"verifyNote":184,"languages":3142,"translateLanguages":24,"viewCount":25,"primaryUrl":3143,"fullTextUrl":24,"authors":3144,"publicationType":389,"publisherRelationship":3265,"citationCount":3319,"citationInfo":3320,"publishDate":3323,"publishYear":3321,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":3324,"openAccess":24,"references":3325,"isForceReanalyzing":570},"9657ec2f-6a04-4eb4-97af-41958fcaaca8","2025-02-09T14:22:15.777+00:00",[],"Mannan-binding-lectin-MBL-associated-serine-protease-1-MASP-1-a-serine-protease-associated-with-humoral-pattern-recognition-molecules-normal-and-acute-phase-levels-in-serum-and-stoichiometry-of-lectin-pathway-components",{"mag":3129,"pmc":3131,"openalex":3133,"abstract":3135,"title":3137,"pm":3139,"doi":3141},{"VOID":3130},"2114563488",{"VOID":3132},"3390472",{"VOID":3134},"W2114563488",{"EN":3136},"\u003Cjats:title>Summary\u003C\u002Fjats:title>\n               \u003Cjats:p>The pattern-recognition molecules mannan-binding lectin (MBL) and the three ficolins circulate in blood in complexes with MBL-associated serine proteases (MASPs). When MBL or ficolin recognizes a microorganism, activation of the MASPs occurs leading to activation of the complement system, an important component of the innate immune system. Three proteins are produced from the MASP1 gene: MASP-1 and MASP-3 and MAp44. We present an assay specific for MASP-1, which is based on inhibition of the binding of anti-MASP-1-specific antibody to MASP-1 domains coated onto microtitre wells. MASP-1 was found in serum in large complexes eluting in a position corresponding to ∼600 kDa after gel permeation chromatography in calcium-containing buffer and as monomers of ∼75 kDa in dissociating buffer. The concentration of MASP-1 in donor sera (n = 105) was distributed log-normally with a median value of 11 µg\u002Fml (range 4–30 µg\u002Fml). Serum and citrate plasma levels were similar, while the values in ethylenediamine tetraacetic acid plasma were slightly lower and in heparin plasma were 1·5 times higher than in serum. MASP-1 was present at adult level at 1 year of age, while it was 60% at birth. In normal healthy individuals the level of MASP-1 was stable throughout a 2-month period. After induction of an acute-phase reaction by operation we found an initial short decrease, concomitant with an increase in C-reactive protein levels, followed by an increase, doubling the MASP-1 concentration after 2 days. The present data prepare the ground for studies on the associations of MASP-1 levels with disease.\u003C\u002Fjats:p>",{"EN":3138},"Mannan-binding lectin (MBL)-associated serine protease-1 (MASP-1), a serine protease associated with humoral pattern-recognition molecules: normal and acute-phase levels in serum and stoichiometry of lectin pathway components",{"VOID":3140},"22670777",{"VOID":3091},[186],"https:\u002F\u002Facademic.oup.com\u002Fcei\u002Farticle\u002F169\u002F1\u002F38\u002F6428952",[3145,3161,3178,3195,3214,3233,3250],{"id":3146,"sortIndex":25,"researcher":24,"roles":3147,"affiliations":3148,"properties":3157,"displayName":2765,"givenName":24,"familyName":24},"f1534f74-e9d9-4fd8-a48a-8b1662ba0bb7",[],[3149],{"id":3150,"sortIndex":25,"affiliation":3151,"properties":24},"6e77f42b-d1ad-4959-aaeb-856b59b6c73c",{"id":3150,"createTime":24,"updateTime":24,"relativeEntities":3152,"slug":24,"properties":3153,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3156,"statistic":24},[],{"title":3154},{"EN":3155},"Department of Biomedicine, Aarhus University, Aarhus",[],{"orcid":3158,"title":3159,"openalex":3160},{"VOID":2763},{"EN":2765},{"VOID":2767},{"id":3162,"sortIndex":104,"researcher":24,"roles":3163,"affiliations":3164,"properties":3171,"displayName":3175,"givenName":24,"familyName":24},"35a2fe7c-b3d8-4890-8c9c-68c4cbcd061f",[],[3165],{"id":3150,"sortIndex":25,"affiliation":3166,"properties":24},{"id":3150,"createTime":24,"updateTime":24,"relativeEntities":3167,"slug":24,"properties":3168,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3170,"statistic":24},[],{"title":3169},{"EN":3155},[],{"orcid":3172,"title":3174,"openalex":3176},{"VOID":3173},"https:\u002F\u002Forcid.org\u002F0000-0001-5425-8689",{"EN":3175},"Louise N. 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