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In this double-blind placebo-controlled study, 40 Chinese female SLE patients taking prednisolone were randomly assigned to receive either monthly oral ibandronate (150 mg) or placebo with daily 1-hydroxycholecalciferol (Alfacalcidol; 1 μg) and calcium supplement for 12 months. Assessments of bone microarchitecture by using HR-pQCT and area bone mineral density (aBMD) of the lumbar spine and hip with dual-energy x-ray absorptiometry (DXA) were performed at baseline and 12 months. No differences in baseline characteristics were found between the two groups. After 12 months, no statistical differences were noted in any of the bone densities, microarchitectural parameters, or percentage changes of these parameters, as measured with HR-pQCT or DXA between the two groups. However, within the active group, the percentage improvement was significant in cortical bone density (P = 0.023) which was absent in the placebo group. Improvement was also seen in the aBMD of both the lumbar spine (P \u003C 0.0001) and the hip (P \u003C 0.005). In the placebo group, the percentage increase in trabecular separation was significant (P = 0.04), and the percentage improvement in aBMD in the spine also was significant (P = 0.049). Oral ibandronate treatment improves microarchitecture in SLE patients taking long-term glucocorticoid assessed with HR-pQCT, and this new technology may have a role in assessing bony changes in future longitudinal studies in SLE patients. ClinicalTrials.gov identifier: NCT00668330.",{"EN":104,"VI":105},"Ibandronate increases cortical bone density in patients with systemic lupus erythematosus on long-term glucocorticoid","Ibandronate làm tăng mật độ xương vỏ ở bệnh nhân mắc lupus ban đỏ hệ thống dùng glucocorticoid kéo dài",{"VOID":107},"Gordon C: Long-term complications of systemic lupus erythematosus. Rheumatology (Oxford). 2002, 41: 1095-1100. 10.1093\u002Frheumatology\u002F41.10.1095.\nKipen Y, Buchbinder R, Forbes A, Strauss B, Littlejohn G, Morand E: Prevalence of reduced bone mineral density in systemic lupus erythematosus and the role of steroids. J Rheumatol. 1997, 24: 1922-1929.\nRamsey-Goldman R, Dunn JE, Huang CF, Dunlop D, Rairie JE, Fitzgerald S, Manzi S: Frequency of fractures in women with systemic lupus erythematosus: comparison with United States population data. Arthritis Rheum. 1999, 42: 882-890. 10.1002\u002F1529-0131(199905)42:5\u003C882::AID-ANR6>3.0.CO;2-C.\nZonana-Nacach A, Barr SG, Magder LS, Petri M: Damage in systemic lupus erythematosus and its association with corticosteroids. Arthritis Rheum. 2000, 43: 1801-1808. 10.1002\u002F1529-0131(200008)43:8\u003C1801::AID-ANR16>3.0.CO;2-O.\nOleksik A, Lips P, Dawson A, Minshall ME, Shen W, Cooper C, Kanis J: Health-related quality of life in postmenopausal women with low BMD with or without prevalent vertebral fractures. J Bone Miner Res. 2000, 15: 1384-1392. 10.1359\u002Fjbmr.2000.15.7.1384.\nHasserius R, Karlsson MK, Nilsson BE, Redlund-Johnell I, Johnell O, European Vertebral Osteoporosis Study: Prevalent vertebral deformities predict increased mortality and increased fracture rate in both men and women: a 10-year population-based study of 598 individuals from the Swedish cohort in the European Vertebral Osteoporosis Study. Osteoporos Int. 2003, 14: 61-68. 10.1007\u002Fs00198-002-1316-9.\nvan Staa TP, Leufkens HG, Cooper C: The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis. Osteoporos Int. 2002, 13: 777-787. 10.1007\u002Fs001980200108.\nvan Staa TP: The pathogenesis, epidemiology and management of glucocorticoid-induced osteoporosis. Calcif Tissue Int. 2006, 79: 129-137. 10.1007\u002Fs00223-006-0019-1.\nBorba VZ, Matos PG, da Silva Viana PR, Fernandes A, Sato EI, Lazaretti-Castro M: High prevalence of vertebral deformity in premenopausal systemic lupus erythematosus patients. Lupus. 2005, 14: 529-533. 10.1191\u002F0961203305lu2154oa.\nBultink IE, Lems WF, Kostense PJ, Dijkmans BA, Voskuyl AE: Prevalence of and risk factors for low bone mineral density and vertebral fractures in patients with systemic lupus erythematosus. Arthritis Rheum. 2005, 52: 2044-2050. 10.1002\u002Fart.21110.\nLi EK, Tam LS, Griffith JF, Zhu TY, Li TK, Li M, Wong KC, Chan M, Lam CW, Chu FS, Wong KK, Leung PC, Kwok A: High prevalence of asymptomatic vertebral fractures in Chinese women with systemic lupus erythematosus. J Rheumatol. 2009, 36: 1646-1652. 10.3899\u002Fjrheum.081337.\nLi EK, Zhu TY, Tam LS, Hung VW, Griffith JF, Li TK, Li M, Wong KC, Leung PC, Kwok AW, Qin L: Bone microarchitecture assessment by high-resolution peripheral quantitative computed tomography in patients with systemic lupus erythematosus on corticosteroids. J Rheumatol. 2010, 37: 1473-1479. 10.3899\u002Fjrheum.091231.\nBoutroy S, Bouxsein ML, Munoz F, Delmas PD: In vivo assessment of trabecular bone microarchitecture by high-resolution peripheral quantitative computed tomography. J Clin Endocrinol Metab. 2005, 90: 6508-6515. 10.1210\u002Fjc.2005-1258.\nSornay-Rendu E, Boutroy S, Munoz F, Delmas PD: Alterations of cortical and trabecular architecture are associated with fractures in postmenopausal women, partially independent of decreased BMD measured by DXA: the OFELY study. J Bone Miner Res. 2007, 22: 425-433. 10.1359\u002Fjbmr.061206.\nSaag KG, Emkey R, Schnitzer TJ, Brown JP, Hawkins F, Goemaere S, Thamsborg G, Liberman UA, Delmas PD, Malice MP, Czachur M, Daifotis AG: Alendronate for the prevention and treatment of glucocorticoid-induced osteoporosis: Glucocorticoid-induced Osteoporosis Intervention Study Group. N Engl J Med. 1998, 339: 292-299. 10.1056\u002FNEJM199807303390502.\nAdachi JD, Bensen WG, Brown J, Hanley D, Hodsman A, Josse R, Kendler DL, Lentle B, Olszynski W, Ste-Marie LG, Tenenhouse A, Chines AA: Intermittent etidronate therapy to prevent corticosteroid-induced osteoporosis. N Engl J Med. 1997, 337: 382-387. 10.1056\u002FNEJM199708073370603.\nReid DM, Hughes RA, Laan RF, Sacco-Gibson NA, Wenderoth DH, Adami S, Eusebio RA, Devogelaer JP: Efficacy and safety of daily risedronate in the treatment of corticosteroid-induced osteoporosis in men and women: a randomized trial: European Corticosteroid-induced Osteoporosis Treatment Study. J Bone Miner Res. 2000, 15: 1006-1013. 10.1359\u002Fjbmr.2000.15.6.1006.\nAmerican College of Rheumatology Ad Hoc Committee on Glucocorticoid-Induced Osteoporosis: Recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis: 2001 update. Arthritis Rheum. 2001, 44: 1496-1503. 10.1002\u002F1529-0131(200107)44:7\u003C1496::AID-ART271>3.0.CO;2-5.\nCohen S, Levy RM, Keller M, Boling E, Emkey RD, Greenwald M, Zizic TM, Wallach S, Sewell KL, Lukert BP, Axelrod DW, Chines AA: Risedronate therapy prevents corticosteroid-induced bone loss: a twelve-month, multicenter, randomized, double-blind, placebo-controlled, parallel-group study. Arthritis Rheum. 1999, 42: 2309-2318. 10.1002\u002F1529-0131(199911)42:11\u003C2309::AID-ANR8>3.0.CO;2-K.\nAdachi JD: Corticosteroid-induced osteoporosis. Int J Fertil Womens Med. 2001, 46: 190-205.\nGonnelli S, Rottoli P, Cepollaro C, Pondrelli C, Cappiello V, Vagliasindi M, Gennari C: Prevention of corticosteroid-induced osteoporosis with alendronate in sarcoid patients. Calcif Tissue Int. 1997, 61: 382-385. 10.1007\u002Fs002239900352.\nAdachi JD, Saag KG, Delmas PD, Liberman UA, Emkey RD, Seeman E, Lane NE, Kaufman JM, Poubelle PE, Hawkins F, Correa-Rotter R, Menkes CJ, Rodriguez-Portales JA, Schnitzer TJ, Block JA, Wing J, McIlwain HH, Westhovens R, Brown J, Melo-Gomes JA, Gruber BL, Yanover MJ, Leite MO, Siminoski KG, Nevitt MC, Sharp JT, Malice MP, Dumortier T, Czachur M, Carofano W, et al: Two-year effects of alendronate on bone mineral density and vertebral fracture in patients receiving glucocorticoids: a randomized, double-blind, placebo-controlled extension trial. Arthritis Rheum. 2001, 44: 202-211. 10.1002\u002F1529-0131(200101)44:1\u003C202::AID-ANR27>3.0.CO;2-W.\nCooper C, Emkey RD, McDonald RH, Hawker G, Bianchi G, Wilson K, Schimmer RC: Efficacy and safety of oral weekly ibandronate in the treatment of postmenopausal osteoporosis. J Clin Endocrinol Metab. 2003, 88: 4609-4615. 10.1210\u002Fjc.2003-022029.\nRinge JD, Dorst A, Faber H, Ibach K, Sorenson F: Intermittent intravenous ibandronate injections reduce vertebral fracture risk in corticosteroid-induced osteoporosis: results from a long-term comparative study. Osteoporosis Int. 2003, 14: 801-807. 10.1007\u002Fs00198-003-1425-0.\nJeffery JR, Leslie WD, Karpinski ME, Nickerson PW, Rush DN: Prevalence and treatment of decreased bone density in renal transplant recipients: a randomized prospective trial of calcitriol versus alendronate. Transplantation. 2003, 76: 1498-1502. 10.1097\u002F01.TP.0000092523.30277.13.\nCohen A, Sambrook P, Shane E: Management of bone loss after organ transplantation. J Bone Miner Res. 2004, 19: 1919-1932. 10.1359\u002Fjbmr.040912.\nReid DM, Devogelaer JP, Saag K, Roux C, Lau CS, Reginster JY, Papanastasiou P, Ferreira A, Hartl F, Fashola T, Mesenbrink P, Sambrook PN, HORIZON investigators: Zoledronic acid and risedronate in the prevention and treatment of glucocorticoid-induced osteoporosis (HORIZON): a multicentre, double-blind, double-dummy, randomised controlled trial. Lancet. 2009, 373: 1253-1263. 10.1016\u002FS0140-6736(09)60250-6.\nMcClung MR, Wasnich RD, Recker R, Cauley JA, Chesnut CH, Ensrud KE, Burdeska A, Mills T, Oral Ibandronate Study Group: Oral daily ibandronate prevents bone loss in early postmenopausal women without osteoporosis. J Bone Miner Res. 2004, 19: 11-18. 10.1359\u002Fjbmr.0301202.\nMcClung MR, Bolognese MA, Sedarati F, Recker RR, Miller PD: Efficacy and safety of monthly oral ibandronate in the prevention of postmenopausal bone loss. Bone. 2009, 44: 418-422. 10.1016\u002Fj.bone.2008.09.011.\nMiller PD, McClung MR, Macovei L, Stakkestad JA, Luckey M, Bonvoisin B, Reginster JY, Recker RR, Hughes C, Lewiecki EM, Felsenberg D, Delmas PD, Kendler DL, Bolognese MA, Mairon N, Cooper C: Monthly oral ibandronate therapy in postmenopausal osteoporosis: 1-year results from the MOBILE study. J Bone Miner Res. 2005, 20: 1315-1322. 10.1359\u002FJBMR.050313.\nReginster JY, Adami S, Lakatos P, Greenwald M, Stepan JJ, Silverman SL, Christiansen C, Rowell L, Mairon N, Bonvoisin B, Drezner MK, Emkey R, Felsenberg D, Cooper C, Delmas PD, Miller PD: Efficacy and tolerability of once-monthly oral ibandronate in postmenopausal osteoporosis: 2 year results from the MOBILE study. Ann Rheum Dis. 2006, 65: 654-661. 10.1136\u002Fard.2005.044958.\nChesnut CH, Ettinger MP, Miller PD, Baylink DJ, Emkey R, Harris ST, Wasnich RD, Watts NB, Schimmer RC, Recker RR: Ibandronate produces significant, similar antifracture efficacy in North American and European women: new clinical findings from BONE. Curr Med Res Opin. 2005, 21: 391-401. 10.1185\u002F030079905X30752.\nRogers MJ: New insights into the molecular mechanisms of action of bisphosphonates. Curr Pharm Des. 2003, 9: 2643-2658. 10.2174\u002F1381612033453640.\nHochberg MC, Chang RW, Dwosh I, Lindsey S, Pincus T, Wolfe F: The American College of Rheumatology 1991 revised criteria for the classification of global functional status in rheumatoid arthritis. Arthritis Rheum. 1992, 35: 498-502. 10.1002\u002Fart.1780350502.\nLynn HS, Lau EM, Au B, Leung PC: Bone mineral density reference norms for Hong Kong Chinese. Osteoporos Int. 2005, 16: 1663-1668. 10.1007\u002Fs00198-005-1899-z.\nHildebrand T, Laib A, Müller R, Dequeker J, Rüegsegger P: Direct three-dimensional morphometric analysis of human cancellous bone: microstructural data from spine, femur, iliac crest, and calcaneus. J Bone Miner Res. 1999, 14: 1167-1174. 10.1359\u002Fjbmr.1999.14.7.1167.\nRinge JD, Cöster A, Meng T, Schacht E, Umbach R: Treatment of glucocorticoid-induced osteoporosis with Alfacalcidol\u002Fcalcium versus vitamin D\u002Fcalcium. Calcif Tissue Int. 1999, 65: 337-340. 10.1007\u002Fs002239900708.\nReginster JY, de Froidmont C, Lecart MP, Sarlet N, Defraigne JO: Alphacalcidol in prevention of glucocorticoid-induced osteoporosis. Calcif Tissue Int. 1999, 65: 328-331. 10.1007\u002Fs002239900706.\nWeinstein RS, Jilka RL, Parfitt AM, Manolagas SC: Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. J Clin Invest. 1998, 102: 274-282. 10.1172\u002FJCI2799.\nDalle Carbonare L, Arlot ME, Chavassieux PM, Roux JP, Portero NR, Meunier PJ: Comparison of trabecular bone microarchitecture and remodeling in glucocorticoid-induced and postmenopausal osteoporosis. J Bone Mienr Res. 2001, 16: 97-103. 10.1359\u002Fjbmr.2001.16.1.97.\nAkahoshi S, Sakai A, Arita S, Ikeda S, Morishita Y, Tsutsumi H, Ito M, Shiraishi A, Nakamura T: Modulation of bone turnover by Alfacalcidol and\u002For alendronate does not prevent glucocorticoid-induced osteoporosis in growing minipigs. J Bone Miner Metab. 2005, 23: 341-350. 10.1007\u002Fs00774-005-0611-x.\nLane NE, Yao W, Balooch M, Nalla RK, Balooch G, Habelitz S, Kinney JH, Bonewald LF: Glucocorticoid-treated mice have localized changes in trabecular bone material properties and osteocyte lacunar size that are not observed in placebo-treated or estrogen-deficient mice. J Bone Miner Res. 2006, 21: 466-476. 10.1359\u002FJBMR.051103.\nBhattoa HP, Bettembuk P, Balogh A, Szegedi G, Kiss E: Bone mineral density in women with systemic lupus erythematosus. Clin Rheumatol. 2002, 21: 135-141. 10.1007\u002Fs10067-002-8272-9.\nChavassieux PM, Arlot ME, Roux JP, Portero N, Daifotis A, Yates AJ, Hamdy NA, Malice MP, Freedholm D, Meunier PJ: Effects of alendronate on bone quality and remodeling in glucocorticoid-induced osteoporosis: a histomorphometric analysis of transiliac biopsies. J Bone Miner Res. 2000, 15: 754-762. 10.1359\u002Fjbmr.2000.15.4.754.\nBorah B, Dufresne TE, Chmielewski PA, Johnson TD, Chines A, Manhart MD: Risedronate preserves bone architecture in postmenopausal women with osteoporosis as measured by three-dimensional microcomputed tomography. Bone. 2004, 34: 736-746. 10.1016\u002Fj.bone.2003.12.013.\nNuzzo S, Lafage-Proust MH, Martin-Badosa E, Boivin G, Thomas T, Alexandre C, Peyrin F: Synchrotron radiation microtomography allows the analysis of three-dimensional microarchitecture and degree of mineralization of human iliac crest biopsy specimens: effects of etidronate treatment. J Bone Miner Res. 2002, 17: 1372-1382. 10.1359\u002Fjbmr.2002.17.8.1372.\nRecker RR, Ste-Marie LG, Langdahl B, Masanauskaite D, Ethgen D, Delmas PD: Oral ibandronate preserves trabecular microarchitecture: micro-computed tomography findings from the oral ibandronate osteoporosis vertebral fracture trial in North America and Europe study. J Clin Densitom. 2009, 12: 71-76. 10.1016\u002Fj.jocd.2008.10.006.\nGreenspan SL, Perera S, Recker R, Wagner JM, Greeley P, Gomberg BR, Seaman P, Kleerekoper M: Changes in trabecular microarchitecture in postmenopausal women on bisphonate therapy. Bone. 2010, 46: 1006-1010. 10.1016\u002Fj.bone.2009.12.025.\nRecker RR, Delmas PD, Halse J, Reid IR, Boonen S, García-Hernandez PA, Supronik J, Lewiecki EM, Ochoa L, Miller P, Hu H, Mesenbrink P, Hartl F, Gasser J, Eriksen EF: Effects of intravenous zoledronic acid once yearly on bone remodeling and bone structure. J Bone Miner Res. 2008, 23: 6-16. 10.1359\u002Fjbmr.070906.\nCohen A, Dempster DW, Müller R, Guo XE, Nickolas TL, Liu XS, Zhang XH, Wirth AJ, van Lenthe GH, Kohler T, McMahon DJ, Zhou H, Rubin MR, Bilezikian JP, Lappe JM, Recker RR, Shane E: Assessment of trabecular and cortical architecture and mechanical competence of bone by high-resolution peripheral computed tomography: comparison with transiliac bone biopsy. Osteoporos Int. 2010, 21: 263-273. 10.1007\u002Fs00198-009-0945-7.\nSekhon K, Kazakia GJ, Burghardt AJ, Hermannsson B, Majumdar S: Accuracy of volumetric bone mineral density measurement in high-resolution peripheral quantitative computed tomography. Bone. 2009, 45: 473-479. 10.1016\u002Fj.bone.2009.05.023.",{"VOID":109},"10.1186\u002Far3170","PUBLICATION","VERIFIED","2025-01-06T22:02:01.494+00:00","Auto Verify",[115],"VI","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Far3170",[118,134,147,163,179,195,209,225,239,253,267,281],{"id":119,"sortIndex":19,"researcher":18,"roles":120,"affiliations":122,"properties":131,"displayName":133,"givenName":18,"familyName":18},"5f8e9719-9dcc-4b7c-ac92-5537331ea97f",[121],"AUTHOR",[123],{"id":124,"sortIndex":19,"affiliation":125,"properties":18},"fe69943e-7b6d-4fd3-b697-d591078eb3cd",{"id":124,"createTime":18,"updateTime":18,"relativeEntities":126,"slug":18,"properties":127,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":130,"statistic":18},[],{"title":128},{"VI":129},"Department of Medicine, The Chinese University of Hong Kong, Prince Wales Hospital, Hong Kong, China",[],{"title":132},{"VI":133},"Edmund K Li",{"id":135,"sortIndex":45,"researcher":18,"roles":136,"affiliations":137,"properties":144,"displayName":146,"givenName":18,"familyName":18},"11e6f950-52b8-4d4e-a87e-96bd8a4a1224",[121],[138],{"id":124,"sortIndex":19,"affiliation":139,"properties":18},{"id":124,"createTime":18,"updateTime":18,"relativeEntities":140,"slug":18,"properties":141,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":143,"statistic":18},[],{"title":142},{"VI":129},[],{"title":145},{"VI":146},"Tracy Y Zhu",{"id":148,"sortIndex":149,"researcher":18,"roles":150,"affiliations":151,"properties":160,"displayName":162,"givenName":18,"familyName":18},"c3ef6073-d1a4-4899-a5b6-b42ba10eab73",2,[121],[152],{"id":153,"sortIndex":19,"affiliation":154,"properties":18},"51041ca4-8035-4209-bcef-5a286dd589f7",{"id":153,"createTime":18,"updateTime":18,"relativeEntities":155,"slug":18,"properties":156,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":159,"statistic":18},[],{"title":157},{"VI":158},"Department of Orthopedics and Traumatology, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China",[],{"title":161},{"VI":162},"Vivian Y Hung",{"id":164,"sortIndex":165,"researcher":18,"roles":166,"affiliations":167,"properties":176,"displayName":178,"givenName":18,"familyName":18},"613bbd9e-35b4-461c-b18b-4923e2f15017",3,[121],[168],{"id":169,"sortIndex":19,"affiliation":170,"properties":18},"774a7c65-3454-44e0-afad-66631ed86862",{"id":169,"createTime":18,"updateTime":18,"relativeEntities":171,"slug":18,"properties":172,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":175,"statistic":18},[],{"title":173},{"VI":174},"Jockey Club Centre of Osteoporosis Care and Control, The Chinese University of Hong Kong, 3\u002FF, School of Public Health, Prince of Wales Hospital, Sha Tin, NT, Hong Kong, China",[],{"title":177},{"VI":178},"Anthony W 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               \u003Cjats:title>Background\n\u003C\u002Fjats:title>\n                \u003Cjats:p>Takayasu arteritis (TAK) is characterized by pro-inflammatory M1 macrophage infiltration and increased interferon (IFN)-γ expression in vascular lesions. IFN-γ is a key cytokine involved in M1 polarization. Macrophage polarization is accompanied by metabolic changes. However, the metabolic regulation mechanism of IFN-γ in M1 macrophage polarization in TAK remains unclear.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Methods\u003C\u002Fjats:title>\n                \u003Cjats:p>Immunohistochemistry and immunofluorescence were employed to observe the expression of IFN-γ, PFKFB3 (6-phosphofructo-2-kinase\u002Ffructose-2,6-biphosphatase 3, the rate-limiting enzyme in glycolysis), and macrophage surface markers in the vascular tissue. Monocyte-derived macrophages from patients with TAK were cultured to examine the role of PFKFB3 in IFN-γ-induced M1 macrophage polarization. Seahorse analysis was used to detect the alterations in glucose metabolism during this process. Quantitative reverse transcription PCR, flow cytometry, and western blot were used to confirm the phenotypes of macrophages and related signaling pathways.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Results\u003C\u002Fjats:title>\n                \u003Cjats:p>In the vascular adventitia of patients with TAK, an increase in PFKFB3 accompanied by IFN-γ expression was observed in M1 macrophages. In vitro, IFN-γ successfully induced macrophage differentiation into the M1 phenotype, which was manifested as an increase in CD80 and HLA-DR markers and the pro-inflammatory cytokines IL-6 and TNF-α. During this process, PFKFB3 expression and glycolysis levels were significantly increased. However, glycolysis and M1 polarization induced by IFN-γ were suppressed by a PFKFB3 inhibitor. In addition, JAK2\u002FSTAT1 phosphorylation was also enhanced in macrophages stimulated by IFN-γ. The effects of IFN-γ on macrophages, including the expression of PFKFB3, glycolysis, and M1 polarization, were also inhibited by the JAK inhibitor tofacitinib or STAT1 inhibitor fludarabine.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Conclusion\u003C\u002Fjats:title>\n                \u003Cjats:p>PFKFB3-mediated glycolysis promotes IFN-γ-induced M1 polarization through the JAK2\u002FSTAT1 signaling pathway, indicating that PFKFB3 plays an important role in M1 polarization mediated by IFN-γ; thus, PFKFB3 is a potential intervention target in TAK.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>",{"EN":331,"VI":332},"Augmented PFKFB3-mediated glycolysis by interferon-γ promotes inflammatory M1 polarization through the JAK2\u002FSTAT1 pathway in local vascular inflammation in Takayasu arteritis","Tăng cường đường phân qua trung gian PFKFB3 bởi interferon-γ thúc đẩy phân cực M1 gây viêm qua con đường JAK2\u002FSTAT1 trong 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Global epidemiology of vasculitis. Nat Rev Rheumatol. 2022;18(1):22–34.",{"doi":486},"10.1038\u002Fs41584-021-00718-8",{"id":18,"text":488,"url":18,"identifiers":489},"Arnaud L, Haroche J, Mathian A, Gorochov G, Amoura Z. Pathogenesis of Takayasu’s arteritis: a 2011 update. Autoimmun Rev. 2011;11(1):61–7.",{"doi":490},"10.1016\u002Fj.autrev.2011.08.001",{"id":18,"text":492,"url":18,"identifiers":493},"Comarmond C, Biard L, Lambert M, Mekinian A, Ferfar Y, Kahn JE, Benhamou Y, Chiche L, Koskas F, Cluzel P, et al. Long-term outcomes and prognostic factors of complications in Takayasu arteritis: a multicenter study of 318 patients. Circulation. 2017;136(12):1114–22.",{"doi":494},"10.1161\u002FCIRCULATIONAHA.116.027094",{"id":18,"text":496,"url":18,"identifiers":497},"Barra L, Yang G, Pagnoux C, Canadian Vasculitis N. Non-glucocorticoid drugs for the treatment of Takayasu’s arteritis: a systematic review and meta-analysis. 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Arthritis Rheum. 1992, 35: 129-137.",{"doi":905},"10.1002\u002Fart.1780350202",{"id":18,"text":907,"url":18,"identifiers":908},"Weinblatt ME, Polisson R, Blotner SD, Sosman JL, Aliabadi P, Baker N, Weissman BN: The effects of drug therapy on radiographic progression of rheumatoid arthritis. Results of a 36-week randomized trial comparing methotrexate and auranofin. Arthritis Rheum. 1993, 36: 613-619.",{"doi":909},"10.1002\u002Fart.1780360507",{"id":18,"text":911,"url":18,"identifiers":912},"Alarcon GS, Kremer JM, Macaluso M, Weinblatt ME, Cannon GW, Palmer WR, St Clair EW, Sunday JS, Alexander RW, Smith GJ, Axiotis CA: Risk factors for methotrexate-induced lung injury in patients with rheumatoid arthritis. A multicenter, case-control study. Methotrexate-Lung Study Group. Ann Intern Med. 1997, 127: 356-364.",{"doi":913},"10.7326\u002F0003-4819-127-5-199709010-00003",{"id":18,"text":915,"url":18,"identifiers":916},"Kremer JM, Furst DE, Weinblatt ME, Blotner SD: Significant changes in serum AST across hepatic histological biopsy grades: prospective analysis of 3 cohorts receiving methotrexate therapy for rheumatoid arthritis. J Rheumatol. 1996, 23: 459-461.",{},{"id":18,"text":918,"url":18,"identifiers":919},"Griffiths RJ: The use of animals in the search for anti-inflammatory drugs. In Mechanisms and Models in Rheumatoid Arthritis. Edited by: Henderson B, Edwards JCW, Pettipher ER. 1995, London: Academic Press, 527-537.",{"doi":920},"10.1016\u002FB978-012340440-4\u002F50060-X",{"id":18,"text":922,"url":18,"identifiers":923},"Wooley PH: Animal models of rheumatoid arthritis. Curr Opin Rheumatol. 1991, 3: 407-420.",{"doi":924},"10.1097\u002F00002281-199106000-00013",{"id":18,"text":926,"url":18,"identifiers":927},"Burkhardt H, Kalden JR: Animal models of autoimmune diseases. Rheumatol Int. 1997, 17: 91-99. 10.1007\u002Fs002960050015.",{"doi":928},"10.1007\u002Fs002960050015",{"id":18,"text":930,"url":18,"identifiers":931},"Wooley PH, Dutcher J, Widmer MB, Gillis S: Influence of a recombinant human soluble tumor necrosis factor receptor FC fusion protein on type II collagen-induced arthritis in mice. J Immunol. 1993, 151: 6602-6607.",{"doi":932},"10.4049\u002Fjimmunol.151.11.6602",{"id":18,"text":934,"url":18,"identifiers":935},"Wooley PH, Whalen JD, Chapman DL, Berger AE, Richard KA, Aspar DG, Staite ND: The effect of an interleukin-1 receptor antagonist protein on type II collagen-induced arthritis and antigen-induced arthritis in mice. Arthritis Rheum. 1993, 36: 1305-1314.",{"doi":936},"10.1002\u002Fart.1780360915",{"id":18,"text":938,"url":18,"identifiers":939},"van den Berg WB, Joosten LA, Helsen M, van de Loo FA: Amelioration of established murine collagen-induced arthritis with anti-IL-1 treatment. Clin Exp Immunol. 1994, 95: 237-243.",{"doi":940},"10.1111\u002Fj.1365-2249.1994.tb06517.x",{"id":18,"text":942,"url":18,"identifiers":943},"Joosten LA, Helsen MM, Saxne T, van de Loo FA, Heinegard D, van den Berg WB: IL-1 alpha beta blockade prevents cartilage and bone destruction in murine type II collagen-induced arthritis, whereas TNF-alpha blockade only ameliorates joint inflammation. J Immunol. 1999, 163: 5049-5055.",{"doi":944},"10.4049\u002Fjimmunol.163.9.5049",{"id":18,"text":946,"url":18,"identifiers":947},"Feldmann M, Brennan FM, Maini RN: Role of cytokines in rheumatoid arthritis. Annu Rev Immunol. 1996, 14: 397-440. 10.1146\u002Fannurev.immunol.14.1.397.",{"doi":948},"10.1146\u002Fannurev.immunol.14.1.397",{"id":18,"text":950,"url":18,"identifiers":951},"Williams RO, Marinova-Mutafchieva L, Feldmann M, Maini RN: Evaluation of TNFα and IL-1 blockade in collagen-induced arthritis and comparison with combined anti-TNFα\u002Fanti-CD4 therapy. J Immunol. 2000, 165: 7240-7245.",{"doi":952},"10.4049\u002Fjimmunol.165.12.7240",{"id":18,"text":954,"url":18,"identifiers":955},"Moreland LW, Schiff MH, Baumgartner SW, Tindall EA, Fleis-chmann RM, Bulpitt KJ, Weaver AL, Keystone EC, Furst DE, Mease PJ, Ruderman EM, Horwitz DA, Arkfeld DG, Garrison L, Burge DJ, Blosch CM, Lange ML, McDonnell ND, Weinblatt ME: Etanercept therapy in rheumatoid arthritis. A randomized, controlled trial. Ann Intern Med. 1999, 130: 478-486.",{"doi":956},"10.7326\u002F0003-4819-130-6-199903160-00004",{"id":18,"text":958,"url":18,"identifiers":959},"Maini R, St Clair EW, Breedveld F, Furst D, Kalden J, Weisman M, Smolen J, Emery P, Harriman G, Feldmann M, Lipsky P: Infliximab (chimeric anti-tumour necrosis factor α monoclonal antibody) versus placebo in rheumatoid arthritis patients receiving concomitant methotrexate: a randomised phase III trial. ATTRACT Study Group. Lancet. 1999, 354: 1932-1939. 10.1016\u002FS0140-6736(99)05246-0.",{"doi":960},"10.1016\u002FS0140-6736(99)05246-0",{"id":18,"text":962,"url":18,"identifiers":963},"Lipsky PE, van der Heijde DM, St Clair EW, Furst DE, Breed-veld FC, Kalden JR, Smolen JS, Weisman M, Emery P, Feld-mann M, Harriman GR, Maini RN: For the Anti-Tumor Necrosis Factor Trial in Rheumatoid Arthritis with Concomitant Therapy Study Group. Infliximab and methotrexate in the treatment of rheumatoid arthritis. N Engl J Med. 2000, 343: 1594-1602. 10.1056\u002FNEJM200011303432202.",{"doi":964},"10.1056\u002FNEJM200011303432202",{"id":18,"text":966,"url":18,"identifiers":967},"Bathon JM, Martin RW, Fleischmann RM, Tesser JR, Schiff MH, Keystone EC, Genovese MC, Wasko MC, Moreland LW, Weaver AL, Markenson J, Finck BK: A comparison of etanercept and methotrexate in patients with early rheumatoid arthritis. N Engl J Med. 2000, 343: 1586-1593. 10.1056\u002FNEJM200011303432201.",{"doi":968},"10.1056\u002FNEJM200011303432201",{"id":18,"text":970,"url":18,"identifiers":971},"Breedveld FC: New insights in the pathogenesis of rheumatoid arthritis. J Rheumatol. 1998, 25 (suppl 53): 3-7.",{},{"id":18,"text":973,"url":18,"identifiers":974},"Smolen JS, Tohidast-Akrad M, Gal A, Kunaver M, Eberl G, Zenz P, Falus A, Steiner G: The role of T-lymphocytes and cytokines in rheumatoid arthritis. Scand J Rheumatol. 1996, 25: 1-4.",{"doi":975},"10.3109\u002F03009749609082660",{"id":977,"createTime":978,"updateTime":979,"relativeEntities":980,"slug":981,"properties":982,"entityType":110,"verifyStatus":111,"verifyTime":991,"verifyNote":113,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":992,"fullTextUrl":18,"authors":993,"publicationType":295,"publisherRelationship":1009,"citationCount":19,"citationInfo":1028,"publishDate":1031,"publishYear":1029,"citationAnalyzeStatus":479,"lastCitationAnalyze":1032,"indexDatabases":1033,"openAccess":18,"references":1034,"isForceReanalyzing":318},"34d62bd3-bde1-448c-8027-def40e4095d2","2024-01-16T12:48:20.751+00:00","2026-08-24T22:03:39.143+00:00",[],"IFN-%CE%B3-transgenic-mice-clues-to-the-pathogenesis-of-systemic-lupus-erythematosus-",{"abstract":983,"title":985,"gsPaper":987,"doi":989},{"EN":984},"Transgenic mice overexpressing IFN-γ in the epidermis develop an inflammatory skin disease resembling cutaneous lupus erythematosus shortly after birth. By 3 months of age, most female transgenics develop a lupus-like syndrome characterised by production of IgG anti-dsDNA, antihistone and antinucleosome autoantibodies. The autoantibodies are nephritogenic, with one-third of females developing a severe immune complex mediated glomerulonephritis. Analysis of these transgenics suggests that pathogenic autoantibodies arise via an antigen-driven T-cell-dependent mechanism with apoptotic keratinocytes acting as a potential source of autoantigen. The mechanism of autoantibody production in IFN-γ transgenics may be relevant to human lupus and is consistent with a central role for cutaneous T cells in the pathogenesis of systemic lupus erythematosus in man.",{"EN":986},"IFN-γ transgenic mice: clues to the pathogenesis of systemic lupus erythematosus?",{"VOID":988},"[\"62851946551299610\"]",{"VOID":990},"10.1186\u002Far124","2024-04-29T06:34:14.307+00:00","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Far124",[994],{"id":995,"sortIndex":19,"researcher":18,"roles":996,"affiliations":997,"properties":1006,"displayName":1008,"givenName":18,"familyName":18},"221a0f37-08e0-4b5b-8fa4-411eac38c6bb",[121],[998],{"id":999,"sortIndex":19,"affiliation":1000,"properties":18},"5c5d964a-492a-4de0-a9d5-86115ef71ea0",{"id":999,"createTime":18,"updateTime":18,"relativeEntities":1001,"slug":18,"properties":1002,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1005,"statistic":18},[],{"title":1003},{"EN":1004},"Imperial Cancer Research Fund, London, UK",[],{"title":1007},{"VI":1008},"John P Seery",{"url":992,"publisher":1010,"properties":1023},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1011,"slug":10,"properties":1012,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1015,"manageAffiliations":1016,"indexDatabases":1017,"url":18,"thumbnailPath":18,"statistic":1018,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"title":1013,"eissn":1014},{"EN":13},{"VOID":15},[],[],[],{"impactFactor":19,"impactFactorByYear":1019,"i10Index":35,"i10IndexLast5Year":36,"totalPublication":37,"totalPublicationByYear":1020,"totalCitation":56,"totalCitationByYear":1021,"totalCitationPerPublication":72,"totalCitationPerPublicationByYear":1022,"hindexLast5Year":89,"hindex":89},{"2012":25,"2013":26,"2015":27,"2016":28,"2017":29,"2018":30,"2019":31,"2020":32,"2021":33,"2022":34,"2023":29},{"1999":39,"2000":40,"2001":41,"2002":42,"2010":43,"2011":44,"2013":45,"2014":46,"2015":47,"2016":48,"2017":49,"2018":50,"2019":51,"2020":49,"2021":52,"2022":53,"2023":54,"2024":55},{"1999":45,"2000":58,"2001":59,"2002":60,"2010":61,"2011":62,"2014":63,"2015":64,"2016":65,"2017":66,"2018":67,"2019":68,"2020":69,"2021":70,"2022":71},{"1999":74,"2000":75,"2001":76,"2002":77,"2010":78,"2011":79,"2014":80,"2015":81,"2016":82,"2017":83,"2018":84,"2019":85,"2020":86,"2021":87,"2022":88},{"pages":1024,"volume":1026},{"VOID":1025},"1-4",{"VOID":1027},"2",{"total":19,"publishYear":1029,"statisticByYear":1030},2000,{},"2000-08-25","2026-08-24T22:03:39.142+00:00",[],[1035,1041,1044,1052,1055,1058,1061,1064,1067,1070,1073,1076,1079,1082,1085,1093,1096,1099,1107,1110,1113,1121,1124,1130,1133,1136,1139,1142,1145],{"id":1036,"text":1037,"url":1038,"identifiers":1039},"4c68646b-0035-4279-8000-0006b275d4fa","Kaplan D: The onset of disease in twins and siblings with systemic lupus erythematosus. J Rheumatol. 1984, 11: 648-652.","https:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs10440-022-00541-7",{"doi":1040},"10.1007\u002Fs10440-022-00541-7",{"id":1036,"text":1042,"url":1038,"identifiers":1043},"Radic MZ, Weigert M: Genetic and structural evidence for antigen selection of anti-DNA antibodies. Ann Rev Immunol. 1994, 12: 487-520.",{"doi":1040},{"id":18,"text":1045,"url":1046,"identifiers":1047},"Walport MJ: Lupus, DNase and defective disposal of cellular debris. Nat Genet. 2000, 25: 135-136. 10.1038\u002F75963.","https:\u002F\u002Fdoi.org\u002F10.1038\u002F75963",{"mag":1048,"openalex":1049,"pm":1050,"doi":1051},"1544561961","W1544561961","10835621","10.1038\u002F75963",{"id":18,"text":1053,"url":18,"identifiers":1054},"Berden JH: Lupus nephritis. Kidney Int. 1997, 52: 538-558.",{},{"id":1036,"text":1056,"url":1038,"identifiers":1057},"Kuroiwa T, Lee EG: Cellular interactions in the pathogenesis of lupus nephritis: the role of T cells and macrophages in the amplification of the inflammatory process in the kidney. Lupus . 1998, 7: 597-603.",{"doi":1040},{"id":18,"text":1059,"url":18,"identifiers":1060},"Graninger WB, Hassfeld W, Pesau BB, Machold KP, Zielinski CC, Smolen JS: Induction of systemic lupus erythemtosus by interferon-gamma in a patient with rheumatoid arthritis. J Rheumatol. 1991, 18: 1621-1622.",{},{"id":1036,"text":1062,"url":1038,"identifiers":1063},"Carroll JM, Crompton T, Seery JP, Watt FM: Transgenic mice expressing IFN-γ in the epidermis have eczema, hair hypopigmentation and hair loss. J Invest Dermatol. 1997, 108: 412-422.",{"doi":1040},{"id":1036,"text":1065,"url":1038,"identifiers":1066},"Carroll JM, Albers KM, Garlick JA, Harrington R, Taichman LB: Tissue-and stratum-specific expression of the human involucrin promoter in transgenic mice. Proc Natl Acad Sci USA. 1993, 90: 10270-10274.",{"doi":1040},{"id":1036,"text":1068,"url":1038,"identifiers":1069},"Seery JP, Carroll JM, Cattell V, Watt FM: Antinuclear autoantibodies and lupus nephritis in transgenic mice expressing interferon γ in the epidermis. J Exp Med. 1997, 186: 1451-1459.",{"doi":1040},{"id":1036,"text":1071,"url":1038,"identifiers":1072},"Sarvetnick N, Shizuru J, Liggitt D, Martin L, McIntyre B, Gregory A, Parslow T, Stewart T: Loss of pancreatic islet tolerance induced by beta-cell expression of interferon-gamma. Nature. 1990, 346: 844-847.",{"doi":1040},{"id":1036,"text":1074,"url":1038,"identifiers":1075},"Gu D, Wogensen L, Calcutt NA, Xia C, Zhu S, Merlie JP, Fox HS, Lindstrom J, Powell HC, Sarvetnick N: Myasthenia gravis-like syndrome induced by expression of interferon γ in the neuromuscular junction. J Exp Med. 1995, 181: 547-557.",{"doi":1040},{"id":1036,"text":1077,"url":1038,"identifiers":1078},"Seery JP, Wang EC, Cattell V, Carroll JM, Owen MJ, Watt FM: A central role for alpha beta T cells in the pathogenesis of murine lupus. J Immunol. 1999, 162: 7241-7248.",{"doi":1040},{"id":1036,"text":1080,"url":1038,"identifiers":1081},"Casciola-Rosen LA, Anhalt G, Rosen A: Autoantigens targeted in systemic lupus erythematosus are clustered in two populations of surface structures on apoptotic keratinocytes. J Exp Med. 1994, 179: 1317-1330.",{"doi":1040},{"id":1036,"text":1083,"url":1038,"identifiers":1084},"Sayama K, Yonehara S, Watanabe Y, Miki Y: Expression of Fas antigen on keratinocytes in vivo and induction of apoptosis in cultured keratinocytes. J Invest Dermatol. 1994, 103: 330-334.",{"doi":1040},{"id":18,"text":1086,"url":1087,"identifiers":1088},"Quignon F, De Bels F, Koken M, Feunteun J, Ameisen JC, de The H: PML induces a novel caspase-independent death process. Nat Genet. 1998, 20: 259-265. 10.1038\u002F3068.","https:\u002F\u002Fdoi.org\u002F10.1038\u002F3068",{"mag":1089,"openalex":1090,"pm":1091,"doi":1092},"2103668513","W2103668513","9806544","10.1038\u002F3068",{"id":1036,"text":1094,"url":1038,"identifiers":1095},"Gaspari AA, Katz SI: Induction and functional characterization of class II MHC (Ia) antigens on murine keratinocytes. J Immunol. 1988, 140: 2956-2963.",{"doi":1040},{"id":1036,"text":1097,"url":1038,"identifiers":1098},"Bal V, McIndoe A, Denton G, Hudson D, Lombardi G, Lamb J, Lechler R: Antigen presentation by keratinocytes induces tolerance in human T cells. Eur J Immunol. 1990, 20: 1893-1897.",{"doi":1040},{"id":18,"text":1100,"url":1101,"identifiers":1102},"Nakajima M, Nakajima A, Kayagaki N, Honda M, Yagita H, Okumura K: Expression of Fas ligand and its receptor in cutaneous lupus: implication in tissue injury. Clin Immunol Immunopathol . 1997, 83: 223-229. 10.1006\u002Fclin.1997.4352.","https:\u002F\u002Fdoi.org\u002F10.1006\u002Fclin.1997.4352",{"mag":1103,"openalex":1104,"pm":1105,"doi":1106},"2060175003","W2060175003","9175910","10.1006\u002Fclin.1997.4352",{"id":1036,"text":1108,"url":1038,"identifiers":1109},"Bennion SD, Middleton MH, David-Bajar KM, Brice S, Norris DA: In three types of interface dermatitis, different patterns of expression of intercellular adhesion molecule-1 (ICAM-1) indicate different triggers of disease. J Invest Dermatol. 1995, 105 (suppl 1): 71S-79S.",{"doi":1040},{"id":1036,"text":1111,"url":1038,"identifiers":1112},"Kind P, Lehmann P, Plewig G: Phototesting in lupus erythematosus. J Invest Dermatol. 1993, 100: 53S-57S.",{"doi":1040},{"id":18,"text":1114,"url":1115,"identifiers":1116},"Pablos JL, Santiago B, Galindo M, Carreira PE, Ballestin C, Gomez-Reino JJ: Keratinocyte apoptosis and p53 expression in cutaneous lupus and dermatomyositis. J Pathol. 1999, 188: 63-68. 10.1002\u002F(SICI)1096-9896(199905)188:1\u003C63::AID-PATH303>3.0.CO;2-E.","https:\u002F\u002Fdoi.org\u002F10.1002\u002F(sici)1096-9896(199905)188:1\u003C63::aid-path303>3.0.co;2-e",{"mag":1117,"openalex":1118,"pm":1119,"doi":1120},"2065145022","W2065145022","10398142","10.1002\u002F(sici)1096-9896(199905)188:1",{"id":1036,"text":1122,"url":1038,"identifiers":1123},"Velthuis PJ, van Weelden H, van Wichen D, Baart de la Faille H: Immunohistopathology of light-induced skin lesions in lupus erythematosus. Acta Derm Venereol. 1990, 70: 93-98.",{"doi":1040},{"id":1125,"text":1126,"url":1127,"identifiers":1128},"7a29abdf-5168-4714-bf6e-7fe1844c549b","Prinz JC, Meurer M, Reiter C, Rieber EP, Plewig G, Riethmuller G: Treatment of severe cutaneous lupus erythematosus with a chimeric CD4 monoclonal antibody, cM-T412. J Am Acad Dermatol. 1996, 34 (2 part 1): 244-252.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0190962296801198",{"doi":1129},"10.1016\u002Fs0190-9622(96)80119-8",{"id":1036,"text":1131,"url":1038,"identifiers":1132},"Robert C, Kupper TS: Inflammatory skin diseases, T cells, and immune surveillance. N Engl J Med. 1999, 24: 1817-1828.",{"doi":1040},{"id":1036,"text":1134,"url":1038,"identifiers":1135},"McGrath H, Martinez-Osuna P, Lee FA: Ultraviolet-A1 (340-400 nm) irradiation therapy in systemic lupus erythematosus. Lupus. 1996, 5: 269-274.",{"doi":1040},{"id":1036,"text":1137,"url":1038,"identifiers":1138},"Casciola-Rosen L, Rosen A: Ultraviolet light-induced keratinocyte apoptosis:a potential mechanism for the induction of skin lesions and autoantibody production in LE. Lupus. 1997, 6: 175-180.",{"doi":1040},{"id":1036,"text":1140,"url":1038,"identifiers":1141},"Venables PJ: Diagnosis and treatment of systemic lupus erythematosus. BMJ. 1993, 307: 663-666.",{"doi":1040},{"id":1036,"text":1143,"url":1038,"identifiers":1144},"Ansel JC, Mountz J, Steinberg AD, DeFabo E, Green I: Effects of UV radiation on autoimmune strains of mice:increased mortality and accelerated autoimmunity in BXSB mice. J Invest Dermatol. 1985, 85: 181-186.",{"doi":1040},{"id":1146,"text":1147,"url":1148,"identifiers":1149},"97efaa55-9e6e-4d8e-a698-633df8703fb9","Nickoloff BJ, Turka LA: Immunological functions of non-professional antigen-presenting cells: new insights from studies of T-cell interactions with keratinocytes. Immunol Today. 1994, 15: 464-469.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002F0167569994901902",{"doi":1150},"10.1016\u002F0167-5699(94)90190-2",{"id":1152,"createTime":1153,"updateTime":1154,"relativeEntities":1155,"slug":1156,"properties":1157,"entityType":110,"verifyStatus":111,"verifyTime":1166,"verifyNote":113,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1167,"fullTextUrl":18,"authors":1168,"publicationType":295,"publisherRelationship":1210,"citationCount":19,"citationInfo":1229,"publishDate":1232,"publishYear":1230,"citationAnalyzeStatus":479,"lastCitationAnalyze":1233,"indexDatabases":1234,"openAccess":18,"references":1235,"isForceReanalyzing":318},"10a08fcf-573b-4ebf-8039-02a91ab2e29f","2024-01-14T01:43:20.911+00:00","2026-08-24T13:53:07.950+00:00",[],"Decreased-microRNA-155-in-Behcet-s-disease-leads-to-defective-control-of-autophagy-thereby-stimulating-excessive-proinflammatory-cytokine-production",{"abstract":1158,"title":1160,"gsPaper":1162,"doi":1164},{"EN":1159},"Earlier, we reported that the microRNA (miR)-155 expression in dendritic cells (DCs) from Behcet’s disease (BD) patients was decreased and affected cytokine production of DCs. In this study, we investigated the mechanisms whereby miR-155 regulates cytokine production by DCs. The formation of autophagosomes in DCs was detected by transmission electron microscopy. Western blotting was used to detect the protein levels of LC3, Beclin-1, P62, p-mTOR, and p-Akt in DCs. TNF-α, IL-6, and IL-1β expression were investigated by ELISA. MiR-155 mimics were transfected to DCs to evaluate its effects on autophagy and cytokine production. RNA interference was used to downregulate the expression of TAB2. The formation of autophagosomes was found in DCs of active BD patients. The expressions of LC3-II, Beclin-1, and P62 were significantly increased in DCs of active BD patients compared to that of inactive BD patients and healthy controls. The expressions of IL-6, IL-1β, and TNF-α were significantly increased in DCs of active BD patients compared to that of healthy controls. The autophagy promoter (3-MA) and inhibitor (rapamycin) significantly decreased or increased the expression of TNF-α, IL-6, and IL-1β by DCs. The expression of LC3-II and Beclin-1 was significantly increased, but the expression of P62 proteins was decreased in DCs transfected with miR-155 mimics or after TAB2 was downregulated. The expression of TNF-α, IL-6, and IL-1β was decreased in DCs after miR-155 was upregulated or TAB2 was downregulated. The ratios of p-Akt\u002FAkt and p-mTOR\u002FmTOR were decreased in DCs after miR-155 was upregulated. These results suggest that miR-155 affects the production of TNF-α, IL-6, and IL-1β by DCs through activation of the Akt\u002FmTOR signaling pathway and by affecting the process of autophagy.",{"EN":1161},"Decreased microRNA-155 in Behcet’s disease leads to defective control of autophagy thereby stimulating excessive proinflammatory cytokine production",{"VOID":1163},"[\"3742378348945416657\"]",{"VOID":1165},"10.1186\u002Fs13075-021-02517-8","2024-05-02T06:28:30.300+00:00","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13075-021-02517-8",[1169,1184,1197],{"id":1170,"sortIndex":19,"researcher":18,"roles":1171,"affiliations":1172,"properties":1181,"displayName":1183,"givenName":18,"familyName":18},"e0b7956d-f34b-45f7-9eb6-6a2e86fa593c",[121],[1173],{"id":1174,"sortIndex":19,"affiliation":1175,"properties":18},"0eb9a11c-9aec-447e-a037-f04cee48d80b",{"id":1174,"createTime":18,"updateTime":18,"relativeEntities":1176,"slug":18,"properties":1177,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1180,"statistic":18},[],{"title":1178},{"VI":1179},"The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Lab of Ophthalmology, Chongqing Eye Institute, Chongqing Branch of National Clinical Research Center for Ocular Diseases, Chongqing, P. R. China",[],{"title":1182},{"VI":1183},"Liang Liang",{"id":1185,"sortIndex":45,"researcher":18,"roles":1186,"affiliations":1187,"properties":1194,"displayName":1196,"givenName":18,"familyName":18},"b8ec4311-2569-4f88-9fc3-f66492ff9e6f",[121],[1188],{"id":1174,"sortIndex":19,"affiliation":1189,"properties":18},{"id":1174,"createTime":18,"updateTime":18,"relativeEntities":1190,"slug":18,"properties":1191,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1193,"statistic":18},[],{"title":1192},{"VI":1179},[],{"title":1195},{"VI":1196},"Qingyun Zhou",{"id":1198,"sortIndex":149,"researcher":18,"roles":1199,"affiliations":1200,"properties":1207,"displayName":1209,"givenName":18,"familyName":18},"dd62ca7f-3fd4-4fd7-bf03-880a6d6d7353",[121],[1201],{"id":1174,"sortIndex":19,"affiliation":1202,"properties":18},{"id":1174,"createTime":18,"updateTime":18,"relativeEntities":1203,"slug":18,"properties":1204,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1206,"statistic":18},[],{"title":1205},{"VI":1179},[],{"title":1208},{"VI":1209},"Lujia Feng",{"url":1167,"publisher":1211,"properties":1224},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1212,"slug":10,"properties":1213,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1216,"manageAffiliations":1217,"indexDatabases":1218,"url":18,"thumbnailPath":18,"statistic":1219,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"title":1214,"eissn":1215},{"EN":13},{"VOID":15},[],[],[],{"impactFactor":19,"impactFactorByYear":1220,"i10Index":35,"i10IndexLast5Year":36,"totalPublication":37,"totalPublicationByYear":1221,"totalCitation":56,"totalCitationByYear":1222,"totalCitationPerPublication":72,"totalCitationPerPublicationByYear":1223,"hindexLast5Year":89,"hindex":89},{"2012":25,"2013":26,"2015":27,"2016":28,"2017":29,"2018":30,"2019":31,"2020":32,"2021":33,"2022":34,"2023":29},{"1999":39,"2000":40,"2001":41,"2002":42,"2010":43,"2011":44,"2013":45,"2014":46,"2015":47,"2016":48,"2017":49,"2018":50,"2019":51,"2020":49,"2021":52,"2022":53,"2023":54,"2024":55},{"1999":45,"2000":58,"2001":59,"2002":60,"2010":61,"2011":62,"2014":63,"2015":64,"2016":65,"2017":66,"2018":67,"2019":68,"2020":69,"2021":70,"2022":71},{"1999":74,"2000":75,"2001":76,"2002":77,"2010":78,"2011":79,"2014":80,"2015":81,"2016":82,"2017":83,"2018":84,"2019":85,"2020":86,"2021":87,"2022":88},{"pages":1225,"volume":1227},{"VOID":1226},"1-11",{"VOID":1228},"23",{"total":19,"publishYear":1230,"statisticByYear":1231},2021,{},"2021-05-06","2026-08-24T13:53:07.949+00:00",[],[1236,1242,1247,1253,1262,1267,1270,1273,1278,1284,1293,1302,1310,1319,1328,1337,1342,1347,1353,1361,1367,1372,1380,1383,1388,1397,1406,1409,1412,1418,1427,1436,1439,1448,1457,1466,1474,1483,1488,1496,1504,1509,1517,1520],{"id":1237,"text":1238,"url":1239,"identifiers":1240},"9aba2c40-6b62-4a94-85b8-8c100d3a2195","Suzuki Kurokawa M, Suzuki N. 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J Biochem. 2012;151(2):157–66. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fjb\u002Fmvr123.","https:\u002F\u002Fdoi.org\u002F10.1093\u002Fjb\u002Fmvr123",{"mag":1470,"openalex":1471,"pm":1472,"doi":1473},"2025843509","W2025843509","21976705","10.1093\u002Fjb\u002Fmvr123",{"id":18,"text":1475,"url":1476,"identifiers":1477},"Criollo A, Niso-Santano M, Malik SA, Michaud M, Morselli E, Mariño G, et al. Inhibition of autophagy by TAB2 and TAB3. EMBO J. 2011;30(24):4908–20. https:\u002F\u002Fdoi.org\u002F10.1038\u002Femboj.2011.413.","https:\u002F\u002Fdoi.org\u002F10.1038\u002Femboj.2011.413",{"mag":1478,"pmc":1479,"openalex":1480,"pm":1481,"doi":1482},"1851347272","3243630","W1851347272","22081109","10.1038\u002Femboj.2011.413",{"id":18,"text":1484,"url":1485,"identifiers":1486},"Niso-Santano M, Criollo A, Malik SA, Michaud M, Morselli E, Mariño G, et al. Direct molecular interactions between Beclin 1 and the canonical NFκB activation pathway. Autophagy. 2012;8(2):268–70. https:\u002F\u002Fdoi.org\u002F10.4161\u002Fauto.8.2.18845.","http:\u002F\u002Fdx.doi.org\u002F10.4161\u002Fauto.8.2.18845",{"doi":1487},"10.4161\u002Fauto.8.2.18845",{"id":18,"text":1489,"url":1490,"identifiers":1491},"Paglin S, Lee NY, Nakar C, Fitzgerald M, Plotkin J, Deuel B, et al. Rapamycin-sensitive pathway regulates mitochondrial membrane potential, autophagy, and survival in irradiated MCF-7 cells. Cancer Res. 2005;65(23):11061–70. https:\u002F\u002Fdoi.org\u002F10.1158\u002F0008-5472.CAN-05-1083.","https:\u002F\u002Fdoi.org\u002F10.1158\u002F0008-5472.can-05-1083",{"mag":1492,"openalex":1493,"pm":1494,"doi":1495},"2141855935","W2141855935","16322256","10.1158\u002F0008-5472.can-05-1083",{"id":18,"text":1497,"url":1498,"identifiers":1499},"Takeuchi H, Kondo Y, Fujiwara K, Kanzawa T, Aoki H, Mills GB, et al. Synergistic augmentation of rapamycin-induced autophagy in malignant glioma cells by phosphatidylinositol 3-kinase\u002Fprotein kinase B inhibitors. Cancer Res. 2005;65(8):3336–46. https:\u002F\u002Fdoi.org\u002F10.1158\u002F0008-5472.CAN-04-3640.","https:\u002F\u002Fdoi.org\u002F10.1158\u002F0008-5472.can-04-3640",{"mag":1500,"openalex":1501,"pm":1502,"doi":1503},"2104381422","W2104381422","15833867","10.1158\u002F0008-5472.can-04-3640",{"id":18,"text":1505,"url":1506,"identifiers":1507},"Okamoto T, Ozawa Y, Kamoshita M, Osada H, Toda E, Kurihara T, et al. The neuroprotective effect of rapamycin as a modulator of the mTOR-NF-kappaB axis during retinal inflammation. Plos one. 2016;11(1):e0146517. https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0146517.","http:\u002F\u002Fdx.doi.org\u002F10.1371\u002Fjournal.pone.0146517",{"doi":1508},"10.1371\u002Fjournal.pone.0146517",{"id":18,"text":1510,"url":1511,"identifiers":1512},"Blair J, Barry R, Moore DJ, Denniston AK. A comprehensive review of mTOR-inhibiting pharmacotherapy for the treatment of non-infectious uveitis. Curr Pharm Des. 2017;23(20):3005–14. https:\u002F\u002Fdoi.org\u002F10.2174\u002F1381612823666170111125550.","https:\u002F\u002Fdoi.org\u002F10.2174\u002F1381612823666170111125550",{"mag":1513,"openalex":1514,"pm":1515,"doi":1516},"2606951408","W2606951408","28078989","10.2174\u002F1381612823666170111125550",{"id":1036,"text":1518,"url":1038,"identifiers":1519},"Blair J, Barry R, Murray PI, Moore DJ, Denniston AK: mTOR-inhibiting pharmacotherapy for the treatment of non-infectious uveitis: a systematic review protocol. Syst Rev. 2018;7(1):83.",{"doi":1040},{"id":18,"text":1521,"url":1522,"identifiers":1523},"Ibrahim MA, Sepah YJ, Watters A, Bittencourt M, Vigil EM, Do DV, et al. One-year outcomes of the SAVE study: sirolimus as a therapeutic approach for UVEitis. Transl Vis Sci Technol. 2015;4(2):4. https:\u002F\u002Fdoi.org\u002F10.1167\u002Ftvst.4.2.4.","https:\u002F\u002Fdoi.org\u002F10.1167\u002Ftvst.4.2.4",{"doi":1524},"10.1167\u002Ftvst.4.2.4",{"id":1526,"createTime":1527,"updateTime":1528,"relativeEntities":1529,"slug":1530,"properties":1531,"entityType":110,"verifyStatus":111,"verifyTime":1540,"verifyNote":113,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1541,"fullTextUrl":18,"authors":1542,"publicationType":295,"publisherRelationship":1695,"citationCount":1714,"citationInfo":1715,"publishDate":1722,"publishYear":1716,"citationAnalyzeStatus":479,"lastCitationAnalyze":1723,"indexDatabases":1724,"openAccess":18,"references":1725,"isForceReanalyzing":318},"e7d9faf0-41f9-4524-800c-86e323568c57","2024-01-22T07:15:37.667+00:00","2026-08-20T03:24:45.488+00:00",[],"Resistance-exercise-improves-physical-fatigue-in-women-with-fibromyalgia-a-randomized-controlled-trial",{"abstract":1532,"title":1534,"gsPaper":1536,"doi":1538},{"EN":1533},"Fibromyalgia (FM) affects approximately 1–3 % of the general population. Fatigue limits the work ability and social life of patients with FM. A few studies of physical exercise have included measures of fatigue in FM, indicating that exercise can decrease fatigue levels. There is limited knowledge about the effects of resistance exercise on multiple dimensions of fatigue in FM. The present study is a sub-study of a multicenter randomized controlled trial in women with FM. The purpose of the present sub-study was to examine the effects of a person-centered progressive resistance exercise program on multiple dimensions of fatigue in women with FM, and to investigate predictors of the potential change in fatigue. A total of 130 women with FM (age 22–64 years) were included in this assessor-blinded randomized controlled multicenter trial examining the effects of person-centered progressive resistance exercise compared with an active control group. The intervention was performed twice a week for 15 weeks. Outcomes were five dimensions of fatigue measured with the Multidimensional Fatigue Inventory (MFI-20). Information about background was collected and the women also completed several health-related questionnaires. Multiple linear stepwise regression was used to analyze predictors of change in fatigue in the total population. A higher improvement was found at the post-treatment examination for change in the resistance exercise group, as compared to change in the active control group in the MFI-20 subscale of physical fatigue (resistance group Δ –1.7, SD 4.3, controls Δ 0.0, SD 2.7, p = 0.013), with an effect size of 0.33. Sleep efficiency was the strongest predictor of change in the MFI-20 subscale general fatigue (beta = −0.54, p = 0.031, R\n                           2 = 0.05). Participating in resistance exercise (beta = 1.90, p = 0.010) and working fewer hours per week (beta = 0.84, p = 0.005) were independent significant predictors of change in physical fatigue (R\n                           2 = 0.14). Person-centered progressive resistance exercise improved physical fatigue in women with FM when compared to an active control group. ClinicalTrials.gov \n                    NCT01226784\n                    \n                  . Registered 21 October 2010.",{"EN":1535},"Resistance exercise improves physical fatigue in women with fibromyalgia: a randomized controlled 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JT. The epidemiology of chronic generalized musculoskeletal pain. Best Pract Res Clin Rheumatol. 2003;17(4):547–61.",{"doi":1040},{"id":1036,"text":1730,"url":1038,"identifiers":1731},"Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, Tugwell P, Campbell SM, Abeles M, Clark P et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33(2):160–72.",{"doi":1040},{"id":1036,"text":1733,"url":1038,"identifiers":1734},"Wolfe F, Ross K, Anderson J, Russell IJ, Hebert L. The prevalence and characteristics of fibromyalgia in the general population. Arthritis Rheum. 1995;38(1):19–28.",{"doi":1040},{"id":1036,"text":1736,"url":1038,"identifiers":1737},"Mease P, Arnold LM, Choy EH, Clauw DJ, Crofford LJ, Glass JM, Martin SA, Morea J, Simon L, Strand CV et al. Fibromyalgia syndrome module at OMERACT 9: domain construct. J Rheumatol. 2009;36(10):2318–29.",{"doi":1040},{"id":1036,"text":1739,"url":1038,"identifiers":1740},"Rohrbeck J, Jordan K, Croft P. The frequency and characteristics of chronic widespread pain in general practice: a case–control study. Br J Gen Pract. 2007;57(535):109–15.",{"doi":1040},{"id":1036,"text":1742,"url":1038,"identifiers":1743},"Mannerkorpi K, Burckhardt CS, Bjelle A. Physical performance characteristics of women with fibromyalgia. Arthritis Care Res. 1994;7(3):123–9.",{"doi":1040},{"id":1036,"text":1745,"url":1038,"identifiers":1746},"Henriksen M, Lund H, Christensen R, Jespersen A, Dreyer L, Bennett RM, Danneskiold-Samsoe B, Bliddal H. Relationships between the fibromyalgia impact questionnaire, tender point count, and muscle strength in female patients with fibromyalgia: a cohort study. Arthritis Rheum. 2009;61(6):732–9.",{"doi":1040},{"id":1036,"text":1748,"url":1038,"identifiers":1749},"Góes SM, Leite N, Shay BL, Homann D, Stefanello JMF, Rodacki ALF. Functional capacity, muscle strength and falls in women with fibromyalgia. Clin Biomech. 2012;27(6):578–83.",{"doi":1040},{"id":1036,"text":1751,"url":1038,"identifiers":1752},"McLoughlin MJ, Colbert LH, Stegner AJ, Cook DB. Are women with fibromyalgia less physically active than healthy women? Med Sci Sports Exerc. 2011;43(5):905–12.",{"doi":1040},{"id":1036,"text":1754,"url":1038,"identifiers":1755},"Alok R, Das SK, Agarwal GG, Tiwari SC, Salwahan L, Srivastava R. Problem-focused coping and self-efficacy as correlates of quality of life and severity of fibromyalgia in primary fibromyalgia patients. J Clin Rheumatol. 2014;20(6):314–6.",{"doi":1040},{"id":1757,"text":1758,"url":1759,"identifiers":1760},"a64b40b9-7255-4b7c-8aeb-14e83e1e2fe0","Wuytack F, Miller P. The lived experience of fibromyalgia in female patients, a phenomenological study. Chiropr Man Therap. 2011;19(1):22.","https:\u002F\u002Fchiromt.biomedcentral.com\u002Farticles\u002F10.1186\u002F2045-709X-19-22",{"doi":1761},"10.1186\u002F2045-709x-19-22",{"id":1036,"text":1763,"url":1038,"identifiers":1764},"Liedberg GM, Henriksson CM. Factors of importance for work disability in women with fibromyalgia: an interview study. Arthritis Rheum. 2002;47(3):266–74.",{"doi":1040},{"id":1036,"text":1766,"url":1038,"identifiers":1767},"Sallinen M, Kukkurainen ML, Peltokallio L, Mikkelsson M. “I’m tired of being tired” - Fatigue as experienced by women with fibromyalgia. Adv Physiother. 2011;13:11–7.",{"doi":1040},{"id":1036,"text":1769,"url":1038,"identifiers":1770},"Wolfe F, Hawley DJ, Wilson K. The prevalence and meaning of fatigue in rheumatic disease. J Rheumatol. 1996;23(8):1407–17.",{"doi":1040},{"id":1036,"text":1772,"url":1038,"identifiers":1773},"Ericsson A, Bremell T, Mannerkorpi K. Usefulness of multiple dimensions of fatigue in fibromyalgia. 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J Rheumatol. 2002;29(5):1041–8.",{"doi":1040},{"id":1036,"text":1952,"url":1038,"identifiers":1953},"Hakkinen A, Hakkinen K, Hannonen P, Alen M. Strength training induced adaptations in neuromuscular function of premenopausal women with fibromyalgia: comparison with healthy women. Ann Rheum Dis. 2001;60(1):21–6.",{"doi":1040},{"id":1036,"text":1955,"url":1038,"identifiers":1956},"Busch AJ, Schachter CL, Overend TJ, Peloso PM, Barber KA. Exercise for fibromyalgia: a systematic review. J Rheumatol. 2008;35(6):1130–44.",{"doi":1040},{"id":1958,"text":1959,"url":1960,"identifiers":1961},"f5619863-3ae1-48a3-938d-0353c1a5e726","Jones KD. Recommendations for resistance training in patients with fibromyalgia. Arthritis Res Ther. 2015;17:258.","http:\u002F\u002Farthritis-research.com\u002Fcontent\u002F17\u002F1\u002F258",{"doi":1962},"10.1186\u002Fs13075-015-0782-3",{"id":1964,"text":1965,"url":1966,"identifiers":1967},"dd3c5599-864d-4392-959f-fc9d71973e59","Nelson NL. Muscle strengthening activities and fibromyalgia: a review of pain and strength outcomes. J Bodyw Mov Ther. 2015;19(2):370–6.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS1360859214001387",{"doi":1968},"10.1016\u002Fj.jbmt.2014.08.007",{"id":1036,"text":1970,"url":1038,"identifiers":1971},"Lindheimer JB, O’Connor PJ, Dishman RK. Quantifying the placebo effect in psychological outcomes of exercise training: a meta-analysis of randomized trials. Sports Med. 2015;45(5):693–711.",{"doi":1040},{"id":1973,"createTime":1974,"updateTime":1975,"relativeEntities":1976,"slug":1977,"properties":1978,"entityType":110,"verifyStatus":111,"verifyTime":1987,"verifyNote":113,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1988,"fullTextUrl":18,"authors":1989,"publicationType":295,"publisherRelationship":2059,"citationCount":19,"citationInfo":2078,"publishDate":2081,"publishYear":2079,"citationAnalyzeStatus":479,"lastCitationAnalyze":2082,"indexDatabases":2083,"openAccess":18,"references":2084,"isForceReanalyzing":318},"311a9d8b-1129-4f9b-8049-f1204b9b647f","2024-02-08T00:33:26.295+00:00","2026-08-15T04:47:43.476+00:00",[],"Absence-of-Epstein-Barr-virus-DNA-in-anti-citrullinated-protein-antibody-expressing-B-cells-of-patients-with-rheumatoid-arthritis",{"abstract":1979,"title":1981,"gsPaper":1983,"doi":1985},{"EN":1980},"Rheumatoid arthritis (RA) is characterized by the presence of disease-specific autoreactive B cell responses, in particular those generating anti-citrullinated protein antibodies (ACPA). For many years, Epstein-Barr virus (EBV) has been implicated in disease pathogenesis, possibly by facilitating the development and persistence of autoreactive B cells. To test this hypothesis, the presence of EBV episomes in ACPA-expressing B cells was analyzed. ACPA-expressing B cells derived from peripheral blood (PB) of seven EBV-seropositive RA patients, and synovial fluid (SF) of one additional EBV-seropositive RA patient, were isolated by flow cytometry. PB cells were expanded for 11–12 days, after which supernatant was harvested and analyzed for cyclic citrullinated-peptide (CCP)2 reactivity. SF cells were isolated directly in a lysis buffer. DNA was isolated and qPCR reactions were performed to determine the EBV status of the cells. EBV-immortalized B cell lymphoblastoid-cell lines (EBV blasts) served as standardized controls. Two hundred ninety-six PB and 60 SF ACPA-expressing B cells were isolated and divided over 16 and 3 pools containing 10–20 cells, respectively. Supernatants of all 16 cultured PB pools contained CCP2-Ig. DNA of all pools was used for qPCR analysis. While EBV-blast analysis showed sensitivity to detect EBV DNA in single B cells, no EBV DNA was detected in any of the ACPA-expressing B cell pools. ACPA-expressing B cells are not enriched for EBV-DNA-containing clones. These results do not support the hypothesis that EBV infection of autoreactive B cells causes or maintains autoreactive B cell populations in RA. Instead, other mechanisms might explain the association between positive EBV serology and RA.",{"EN":1982},"Absence of Epstein-Barr virus DNA in anti-citrullinated protein antibody-expressing B cells of patients with rheumatoid arthritis",{"VOID":1984},"[\"18363597252386687890\"]",{"VOID":1986},"10.1186\u002Fs13075-022-02919-2","2024-04-30T13:42:25.629+00:00","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13075-022-02919-2",[1990,2005,2018,2033,2046],{"id":1991,"sortIndex":19,"researcher":18,"roles":1992,"affiliations":1993,"properties":2002,"displayName":2004,"givenName":18,"familyName":18},"56527e38-4de6-4b64-8e71-548f66c58242",[121],[1994],{"id":1995,"sortIndex":19,"affiliation":1996,"properties":18},"16da85ab-dd1c-40ea-9f1b-514cb67385e4",{"id":1995,"createTime":18,"updateTime":18,"relativeEntities":1997,"slug":18,"properties":1998,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2001,"statistic":18},[],{"title":1999},{"VI":2000},"Department of Rheumatology, Leiden University Medical Center, Leiden, the Netherlands",[],{"title":2003},{"VI":2004},"Sanne Kroos",{"id":2006,"sortIndex":45,"researcher":18,"roles":2007,"affiliations":2008,"properties":2015,"displayName":2017,"givenName":18,"familyName":18},"95d5ab94-4c5b-4cef-909f-c69e907aced0",[121],[2009],{"id":1995,"sortIndex":19,"affiliation":2010,"properties":18},{"id":1995,"createTime":18,"updateTime":18,"relativeEntities":2011,"slug":18,"properties":2012,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2014,"statistic":18},[],{"title":2013},{"VI":2000},[],{"title":2016},{"VI":2017},"Arieke S. 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From risk to chronicity: evolution of autoreactive B cell and antibody responses in rheumatoid arthritis. Nat Rev Rheumatol. 2022;18:371.",{"doi":1040},{"id":1036,"text":2089,"url":1038,"identifiers":2090},"Smatti MK, Al-Sadeq DW, Ali NH, Pintus G, Abou-Saleh H, Nasrallah GK. Epstein-Barr Virus Epidemiology, Serology, and Genetic Variability of LMP-1 Oncogene Among Healthy Population: An Update. Front Oncol. 2018;8:211.",{"doi":1040},{"id":18,"text":2092,"url":18,"identifiers":2093},"Laichalk LL, Hochberg D, Babcock GJ, Freeman RB, Thorley-Lawson DA. The Dispersal of Mucosal Memory B Cells: Evidence from Persistent EBV Infection. Immunity. 2002;16:745–54.",{},{"id":2095,"text":2096,"url":2097,"identifiers":2098},"2848dbbd-c10f-4702-b9d3-55a8f469755e","Balandraud N, Roudier J. Epstein-Barr virus and rheumatoid arthritis. Joint Bone Spine. 2018;85(2):165–70.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS1297319X17300933",{"doi":2099},"10.1016\u002Fj.jbspin.2017.04.011",{"id":2101,"text":2102,"url":2103,"identifiers":2104},"8d666dcb-8a6a-439a-8003-b2c3d4a5d518","Swanson-Mungerson M, Longnecker R. Epstein-Barr virus latent membrane protein 2A and autoimmunity. Trends Immunol. 2007;28(5):213–8.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS1471490607000701",{"doi":2105},"10.1016\u002Fj.it.2007.03.002",{"id":1036,"text":2107,"url":1038,"identifiers":2108},"He B, Raab-Traub N, Casali P, Cerutti A. EBV-encoded latent membrane protein 1 cooperates with BAFF\u002FBLyS and APRIL to induce T cell-independent Ig heavy chain class switching. J Immunol. 2003;171(10):5215–24.",{"doi":1040},{"id":1036,"text":2110,"url":1038,"identifiers":2111},"Croia C, Serafini B, Bombardieri M, Kelly S, Humby F, Severa M, et al. Epstein-Barr virus persistence and infection of autoreactive plasma cells in synovial lymphoid structures in rheumatoid arthritis. Ann Rheum Dis. 2013;72(9):1559–68.",{"doi":1040},{"id":1036,"text":2113,"url":1038,"identifiers":2114},"Kerkman PF, Fabre E, van der Voort EI, Zaldumbide A, Rombouts Y, Rispens T, et al. Identification and characterisation of citrullinated antigen-specific B cells in peripheral blood of patients with rheumatoid arthritis. Ann Rheum Dis. 2016;75(6):1170–6.",{"doi":1040},{"id":1036,"text":2116,"url":1038,"identifiers":2117},"Kissel T, Reijm S, Slot LM, Cavallari M, Wortel CM, Vergroesen RD, et al. Antibodies and B cells recognising citrullinated proteins display a broad cross-reactivity towards other post-translational modifications. Ann Rheum Dis. 2020;79(4):472–80.",{"doi":1040},{"id":18,"text":2119,"url":18,"identifiers":2120},"Kraal LJN, Nijland ML, Germar KL, Baeten DLP, Ten Berge IJM, Fehres CM. Anti-citrullinated protein antibody response after primary EBV infection in kidney transplant patients. PLoS One. 2018;13(5):e0197219.",{},{"id":1036,"text":2122,"url":1038,"identifiers":2123},"Stevens SJC, Vervoort MBHJ, van den Brule AJC, Meenhorst PL, Meijer CJLM, Middeldorp JM. Monitoring of Epstein-Barr Virus DNA Load in Peripheral Blood by Quantitative Competitive PCR. J Clin Microbiol. 1999;37(9):2852–7.",{"doi":1040},{"id":1036,"text":2125,"url":1038,"identifiers":2126},"Balandraud N, Meynard JB, Auger I, Sovran H, Mugnier B, Reviron D, et al. Epstein-Barr virus load in the peripheral blood of patients with rheumatoid arthritis: accurate quantification using real-time polymerase chain reaction. Arthritis Rheum. 2003;48(5):1223–8.",{"doi":1040},{"id":1036,"text":2128,"url":1038,"identifiers":2129},"Westergaard MW, Draborg AH, Troelsen L, Jacobsen S, Houen G. Isotypes of Epstein-Barr virus antibodies in rheumatoid arthritis: association with rheumatoid factors and citrulline-dependent antibodies. Biomed Res Int. 2015;2015:472174.",{"doi":1040},{"id":1036,"text":2131,"url":1038,"identifiers":2132},"Baboonian C, Venables PJW, Williams DG, Williams RO, Maini RN. Cross reaction of antibodies to a glycine\u002Falanine repeat sequence of Epstein-Barr virus nuclear antigen-1 with collagen, cytokeratin, and actin. Ann Rheum Dis. 1991;50:772–5.",{"doi":1040},{"id":1036,"text":2134,"url":1038,"identifiers":2135},"Cornillet M, Verrouil E, Cantagrel A, Serre G, Nogueira L. In ACPA-positive RA patients, antibodies to EBNA35-58Cit, a citrullinated peptide from the Epstein-Barr nuclear antigen-1, strongly cross-react with the peptide beta60-74Cit which bears the immunodominant epitope of citrullinated fibrin. Immunol Res. 2015;61(1-2):117–25.",{"doi":1040},{"id":1036,"text":2137,"url":1038,"identifiers":2138},"Fanelli I, Rovero P, Hansen PR, Frederiksen JL, Houen G, Trier NH. Reactivity of Rheumatoid Arthritis-Associated Citrulline-Dependent Antibodies to Epstein-Barr Virus Nuclear Antigen1-3. Antibodies. 2022;11:20.",{"doi":1040},{"id":1036,"text":2140,"url":1038,"identifiers":2141},"Lanz TV, Brewer RC, Ho PP, Moon JS, Jude KM, Fernandez D, et al. Clonally expanded B cells in multiple sclerosis bind EBV EBNA1 and GlialCAM. Nature. 2022;603(7900):321–7.",{"doi":1040},{"id":2143,"createTime":2144,"updateTime":2145,"relativeEntities":2146,"slug":2147,"properties":2148,"entityType":110,"verifyStatus":111,"verifyTime":2157,"verifyNote":113,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":2158,"fullTextUrl":18,"authors":2159,"publicationType":295,"publisherRelationship":2547,"citationCount":19,"citationInfo":2566,"publishDate":2569,"publishYear":2567,"citationAnalyzeStatus":479,"lastCitationAnalyze":2570,"indexDatabases":2571,"openAccess":18,"references":2572,"isForceReanalyzing":318},"24a71a5a-a705-4031-8064-bd0017c91bc0","2024-02-06T10:22:29.280+00:00","2026-08-14T07:41:08.708+00:00",[],"Early-changes-in-gene-expression-and-inflammatory-proteins-in-systemic-juvenile-idiopathic-arthritis-patients-on-canakinumab-therapy",{"abstract":2149,"title":2151,"gsPaper":2153,"doi":2155},{"EN":2150},"Canakinumab is a human anti-interleukin-1β (IL-1β) monoclonal antibody neutralizing IL-1β-mediated pathways. We sought to characterize the molecular response to canakinumab and evaluate potential markers of response using samples from two pivotal trials in systemic juvenile idiopathic arthritis (SJIA). Gene expression was measured in patients with febrile SJIA and in matched healthy controls by Affymetrix DNA microarrays. Transcriptional response was assessed by gene expression changes from baseline to day 3 using adapted JIA American College of Rheumatology (aACR) response criteria (50 aACR JIA). Changes in pro-inflammatory cytokines IL-6 and IL-18 were assessed up to day 197. Microarray analysis identified 984 probe sets differentially expressed (≥2-fold difference; P \u003C 0.05) in patients versus controls. Over 50% of patients with ≥50 aACR JIA were recognizable by baseline expression values. Analysis of gene expression profiles from patients achieving ≥50 aACR JIA response at day 15 identified 102 probe sets differentially expressed upon treatment (≥2-fold difference; P \u003C 0.05) on day 3 versus baseline, including IL-1β, IL-1 receptors (IL1-R1 and IL1-R2), IL-1 receptor accessory protein (IL1-RAP), and IL-6. The strongest clinical response was observed in patients with higher baseline expression of dysregulated genes and a strong transcriptional response on day 3. IL-6 declined by day 3 (≥8-fold decline; P \u003C 0.0001) and remained suppressed. IL-18 declined on day 57 (≥1.5-fold decline, P ≤ 0.002). Treatment with canakinumab in SJIA patients resulted in downregulation of innate immune response genes and reductions in IL-6 and clinical symptoms. Additional research is needed to investigate potential differences in the disease mechanisms in patients with heterogeneous gene transcription profiles. Clinicaltrials.gov: \n                    NCT00886769\n                    \n                   (trial 1). Registered on 22 April 2009; \n                    NCT00889863\n                    \n                   (trial 2). 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