Polymyositis (PM) is a chronic autoimmune inflammatory myopathy affecting striated muscles (1). An accumulated body of evidence supports the notion that the pathology of PM is driven by cytotoxic CD8 T cells (2-7), but the event that initiates the inflammatory processes has not been identified. Currently, patients with PM are treated primarily with nonspecific immunosuppressants, including high-dose corticosteroids, methotrexate, and/or other small-molecule immunosuppressants. Because the administration of therapeutic agents can elicit a wide variety of adverse reactions, treatments that address the specific pathology of PM need to be developed.In the development of new therapeutic approaches to human diseases, animal models have served as a means with which to identify therapeutic targets and to test the effect of new treatments (8-11). Despite the known limitations, experiments in animals with collagen-induced arthritis (CIA) have facilitated development of new treatments for rheumatoid arthritis (RA). Treatment approaches such as blockade of interleukin-1 (IL-1), tumor necrosis factor ␣ (TNF␣), and IL-6 have had an enormous effect in modulating the disease course of RA (12-15).However, in myositis research, no appropriate