{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T06:44:20Z","timestamp":1774507460975,"version":"3.50.1"},"reference-count":32,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2021,7,7]],"date-time":"2021-07-07T00:00:00Z","timestamp":1625616000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81770696 to KL"],"award-info":[{"award-number":["81770696 to KL"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81970596 to KL"],"award-info":[{"award-number":["81970596 to KL"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Arthritis &amp; Rheumatology"],"published-print":{"date-parts":[[2021,8]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>Collectin 11 (CL\u201011) is a soluble C\u2010type lectin, a mediator of innate immunity. Its role in autoimmune disorders is unknown. We undertook this study to determine the role of CL\u201011 in a mouse model of rheumatoid arthritis (RA).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A murine collagen\u2010induced arthritis (CIA) model was used and combined two approaches, including gene deletion of <jats:italic>Colec11<\/jats:italic> and treatment with recombinant CL\u201011 (rCL\u201011). Joint inflammation and tissue destruction, circulating levels of inflammatory cytokines, and adaptive immune responses were assessed in mice with CIA. Splenic CD11c+ cells were used to examine the influence of CL\u201011 on antigen\u2010presenting cell (APC) function. Serum CL\u201011 levels in RA patients were also examined.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>Colec11<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice developed more severe arthritis than wild\u2010type mice, as determined by disease incidence, clinical arthritis scores, and histopathology (<jats:italic>P<\/jats:italic> &lt; 0.05). Disease severity was associated with significantly enhanced APC activation, Th1\/Th17 responses, pathogenic IgG2a production and joint inflammation, as well as elevated circulating levels of inflammatory cytokines. In vitro analysis of CD11c+ cells revealed that CL\u201011 is critical for suppression of APC activation and function. Pharmacologic treatment of mice with rCL\u201011 reduced the severity of CIA in mice. Analysis of human blood samples revealed that serum CL\u201011 levels were lower in RA patients (n = 51) compared to healthy controls (n = 53). Reduction in serum CL\u201011 was inversely associated with the Disease Activity Score in 28 joints, erythrocyte sedimentation rate, and C\u2010reactive protein level (<jats:italic>P<\/jats:italic> &lt; 0.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our findings demonstrate a novel role of CL\u201011 in protection against RA, suggesting that the underlying mechanism involves suppression of APC activation and subsequent T cell responses.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.41696","type":"journal-article","created":{"date-parts":[[2021,2,20]],"date-time":"2021-02-20T17:15:24Z","timestamp":1613841324000},"page":"1430-1440","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Protective Role of Collectin 11 in a Mouse Model of Rheumatoid Arthritis"],"prefix":"10.1002","volume":"73","author":[{"given":"Na","family":"Wang","sequence":"first","affiliation":[{"name":"The Second 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