{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T13:05:30Z","timestamp":1790859930190,"version":"4.1.0"},"reference-count":56,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2019,3,23]],"date-time":"2019-03-23T00:00:00Z","timestamp":1553299200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81772326"],"award-info":[{"award-number":["81772326"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FEBS Journal"],"published-print":{"date-parts":[[2019,5]]},"abstract":"\n Synovitis, the chronic inflammation of the synovial membranes, is a hallmark of rheumatoid arthritis, a chronic disease with profound impact on human health. Recently, interleukin\u201035 (\n IL<\/jats:styled-content>\n \u201035), a new member of the\n IL<\/jats:styled-content>\n \u201012 family, was identified as an anti\u2010inflammatory and immunosuppressive cytokine and was shown to ameliorate collagen\u2010induced arthritis (\n CIA<\/jats:styled-content>\n ) in mice. However, the mechanism by which\n IL<\/jats:styled-content>\n \u201035 alleviates\n CIA<\/jats:styled-content>\n remains unknown. In this study, we investigated the effect of\n IL<\/jats:styled-content>\n \u201035 on the\n CIA<\/jats:styled-content>\n microenvironment and, specifically, the tumor necrosis factor alpha (\n TNF<\/jats:styled-content>\n \u2010\u03b1)\u2010induced macrophage inflammatory response and apoptosis of fibroblast\u2010like synoviocytes (\n FLSs<\/jats:styled-content>\n ). Firstly, using\n RT<\/jats:styled-content>\n \u2010\n PCR<\/jats:styled-content>\n , western blot, and flow cytometry, we found that\n IL<\/jats:styled-content>\n \u201035 suppressed\n TNF<\/jats:styled-content>\n \u2010\u03b1\u2010induced inflammatory responses by down\u2010regulating\n iNOS<\/jats:styled-content>\n and\n COX<\/jats:styled-content>\n \u20102 in peripheral blood monocyte\u2010derived macrophages.\n IL<\/jats:styled-content>\n \u201035 also activated alternative M2 macrophage polarization, as determined by evaluation of\n CCR<\/jats:styled-content>\n 7 and\n CD<\/jats:styled-content>\n 206 expression. Moreover, we showed that\n IL<\/jats:styled-content>\n \u201035 enhanced\n TNF<\/jats:styled-content>\n \u2010\u03b1\u2010induced\n FLS<\/jats:styled-content>\n apoptosis. Using a panel of immunohistochemical and immunofluorescence analyses in a\n CIA<\/jats:styled-content>\n model established in 18\n DBA<\/jats:styled-content>\n \/1J mice, we demonstrated that\n IL<\/jats:styled-content>\n \u201035 promotes synoviocyte apoptosis and alternative activation of macrophages to alleviate arthritis\n in vivo<\/jats:italic>\n . Taken together, our results show that\n IL<\/jats:styled-content>\n \u201035 promotes\n TNF<\/jats:styled-content>\n \u2010\u03b1\u2010induced\n FLS<\/jats:styled-content>\n apoptosis and modulates M2 macrophage polarization to ameliorate\n CIA<\/jats:styled-content>\n inflammation both\n in vitro<\/jats:italic>\n and\n in vivo<\/jats:italic>\n .\n <\/jats:p>","DOI":"10.1111\/febs.14801","type":"journal-article","created":{"date-parts":[[2019,3,5]],"date-time":"2019-03-05T01:47:38Z","timestamp":1551750458000},"page":"1972-1985","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["IL<\/scp>\n \u201035 ameliorates collagen\u2010induced arthritis by promoting\n TNF<\/scp>\n \u2010\u03b1\u2010induced apoptosis of synovial fibroblasts and stimulating M2 macrophages polarization"],"prefix":"10.1111","volume":"286","author":[{"given":"Mingzheng","family":"Peng","sequence":"first","affiliation":[{"name":"Shanghai Key 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Surgery Shanghai Ninth People's Hospital Affiliated Shanghai Jiao Tong University School of Medicine China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinwu","family":"Wang","sequence":"additional","affiliation":[{"name":"Shanghai Key Laboratory of Orthopaedic Implant Department of Orthopaedic Surgery Shanghai Ninth People's Hospital Affiliated Shanghai Jiao Tong University School of Medicine China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2019,3,23]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.pop.2018.02.010"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s40273-014-0174-6"},{"key":"e_1_2_9_4_1","first-page":"175","article-title":"One year in review 2018: pathogenesis of rheumatoid arthritis","volume":"36","author":"Calabresi E","year":"2018","journal-title":"Clin Exp 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