{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:19:38Z","timestamp":1791299978259,"version":"4.1.0"},"reference-count":49,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2007,3,29]],"date-time":"2007-03-29T00:00:00Z","timestamp":1175126400000},"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":[[2007,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>To establish a new murine model of polymyositis (PM) for the understanding of its pathologic mechanisms and the development of new treatment strategies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>C protein\u2013induced myositis (CIM) was induced by a single immunization of recombinant human skeletal C protein in C57BL\/6 mice, as well as in CD4\u2010depleted, CD8\u2010depleted, and mutant mice as controls. Some mice were treated with high\u2010dose intravenous immunoglobulin (IVIG) after disease induction. Muscle tissues were examined histologically.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In mice with CIM, inflammation was confined to the skeletal muscles. Histologic examination revealed a common pathologic feature of CIM and PM, involving abundant infiltration of CD8 and perforin\u2010expressing cells in the endomysial site of the injured muscle. Suppression of myositis was achieved by depletion of both CD4 and CD8 T cells. Despite the development of serum anti\u2013C protein antibodies in wild\u2010type mice, severe myositis was induced in mice deficient in B cells. Induction of myositis was suppressed in interleukin\u20101\u03b1\/\u03b2 (IL\u20101\u03b1\/\u03b2)\u2013null mutant mice, but not in tumor necrosis factor \u03b1 (TNF\u03b1)\u2013null mutant mice. Use of IVIG, a treatment with proven efficacy in PM, suppressed CIM in the subgroup of treated mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>CIM mimics PM pathologically and clinically. Infiltration of CD8 T cells is the most likely mechanism of muscle injury, and IL\u20101, but not B cells or TNF\u03b1, is crucial in the development of CIM. IVIG has therapeutic effects in CIM, suggesting that the effects of IVIG are not mediated by suppression of antibody\u2010mediated tissue injury. This murine model provides a useful tool for understanding the pathologic mechanisms of PM and for developing new treatment strategies.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.22521","type":"journal-article","created":{"date-parts":[[2007,3,29]],"date-time":"2007-03-29T16:18:31Z","timestamp":1175185111000},"page":"1304-1314","source":"Crossref","is-referenced-by-count":69,"title":["A new murine model to define the critical pathologic and therapeutic mediators of 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