Experimental allergic myositis (EAM) was produced in SJL/J mice by inoculation with the myosin B fraction of the rabbit skeletal muscle, and the pathological changes were quantified. The myosin B fraction contains actin, myosin, tropomyosin and many other proteins, and has been known to induce severe EAM in guinea pigs. In the present model, macrophages and CD4+ lymphocytes predominated among the infiltrating cells. On the surface of muscle fibers and in the regions of cell infiltration deposition of the immunoglobulin G (IgG) and complement factor 3 was observed. EAM was transferred to normal mice by injecting the serum IgG of EAM. Depleting the recipients of complement before the transfer resulted in less-severe pathological changes. Morphologically, the EAM IgG showed an affinity for the nuclei, myofilaments, sarcolemma and blood vessels of mouse skeletal muscle. Biochemically EAM IgG contained antibodies against myosin, actin, troponin, M protein and other muscle proteins. These results indicated that IgG and complement play important roles in this model.