{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,11]],"date-time":"2026-07-11T11:07:32Z","timestamp":1783768052737,"version":"3.55.0"},"reference-count":51,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,2,25]],"date-time":"2013-02-25T00:00:00Z","timestamp":1361750400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2013,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Murine collagen antibody\u2013induced arthritis (CAIA), like collagen\u2010induced arthritis, has clinical and immunopathologic features that parallel those in human rheumatoid arthritis (RA). This study was undertaken to examine the effects of autoantibodies to type II collagen (CII) on articular cartilage in the paws of mice, under conditions in which other factors that may influence joint pathology could be excluded.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Mice of 2 different strains, B10.QC5\u03b4 and the parental strain B10.Q, were injected intravenously with either saline or arthritogenic monoclonal antibodies (mAb) to CII. B10.QC5\u03b4 mice lack complement factor C5 and do not develop CAIA when injected with arthritogenic mAb, whereas B10.Q mice have C5 and develop CAIA when administered the mAb and a subsequent injection of lipopolysaccharide. Three days after injection the paws of the mice were examined by standard histologic methods to assess morphologic appearance and proteoglycan loss, and by synchrotron\u2010enhanced Fourier transform infrared microspectroscopy to assess chemical evidence of structural change.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>No macroscopic or microscopic signs of inflammation were evident in the mice. However, in contrast to the saline\u2010injected controls, all mAb\u2010injected mice exhibited cartilage damage in all joints, with loss of proteoglycans and collagen, chondrocyte hyperplasia and\/or loss, and surface damage in the interphalangeal joints.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The implication of these findings is that an autoimmune response to CII can disrupt articular cartilage, particularly that of the small joints, and the subsequent integrity of the cartilage depends on a balance between breakdown and repair. This has relevance with regard to RA, in which such autoantibodies occur but the inflammatory response may dominate clinically and mask underlying features of the autoimmune response.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.37805","type":"journal-article","created":{"date-parts":[[2012,12,13]],"date-time":"2012-12-13T18:58:36Z","timestamp":1355425116000},"page":"650-659","source":"Crossref","is-referenced-by-count":25,"title":["Type II collagen\u2013specific antibodies induce cartilage damage in mice independent of inflammation"],"prefix":"10.1002","volume":"65","author":[{"given":"Allyson M.","family":"Croxford","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Senga","family":"Whittingham","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donald","family":"McNaughton","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kutty 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