{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T23:27:05Z","timestamp":1792106825434,"version":"4.4.0"},"reference-count":50,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2009,7,30]],"date-time":"2009-07-30T00:00:00Z","timestamp":1248912000000},"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":[[2009,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>To explore new molecular targets in the treatment of polymyositis (PM) by examining a recently established murine model of PM, C protein\u2013induced myositis (CIM), for involvement of an interleukin\u20106 (IL\u20106)\/IL\u201017A pathway.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>CIM was induced by immunizing wild\u2010type mice as well as IL\u20106\u2013null and IL\u201017A\u2013null C57BL\/6 mice with recombinant mouse skeletal C protein fragments. Some mice were treated with anti\u2013IL\u20106 receptor (anti\u2013IL\u20106R) monoclonal antibodies or control antibodies. Muscle tissue samples were examined histologically and immunohistochemically.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The syngeneic C protein fragments successfully induced inflammation in the skeletal muscles of wild\u2010type mice. IL\u20106 was expressed by mononuclear cells, especially in macrophages, infiltrating in the muscles. IL\u20106\u2013null mice developed myositis with significantly lower incidence and milder severity than wild\u2010type mice. In contrast, IL\u201017A\u2013null mice were as susceptible to CIM as wild\u2010type mice. Intraperitoneal administration of anti\u2013IL\u20106R monoclonal antibodies, but not of control monoclonal antibodies, ameliorated CIM both preventively and therapeutically.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our findings indicate that IL\u20106 is critically involved in the development of CIM. Although many other autoimmune models require IL\u20106 for differentiation of pathogenic T cells producing IL\u201017A, IL\u201017A was dispensable in CIM. Nevertheless, treatment with anti\u2013IL\u20106R antibodies was effective. IL\u20106 blockade is potentially a new approach to the treatment of autoimmune myositis, via processes distinct from interference in the IL\u20106\/IL\u201017A pathway.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.24689","type":"journal-article","created":{"date-parts":[[2009,7,30]],"date-time":"2009-07-30T15:15:42Z","timestamp":1248966942000},"page":"2505-2512","source":"Crossref","is-referenced-by-count":92,"title":["Therapeutic effects of interleukin\u20106 blockade in a murine model of polymyositis that does not require 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