von Kreuter B F, Santos-Buch C A
Clin Exp Rheumatol. 1986 Jan-Mar;4(1):83-9.
The pathogenic mechanisms related to the development of idiopathic inflammatory skeletal muscle disease are unknown. The myotropic protozoa Trypanosoma cruzi and Toxoplasma gondii are implicated in the induction of myositis in experimental animals (1) and humans (2). In the experiments reported here, a model of pathoimmune myositis is described in C3H/HeJ T. cruzi-infecteéd mice. The results showed a significant occurrence of acquired, T. cruzi antigen-dependent spleen T cell cytotoxicity to syngeneic skeletal muscle myoblasts of C3H mice which developed an apparently sterile lymphoid polymyositis. Further experiments with polymyositic C3H mice suggest that spleen B cells do not secrete antibody capable of inducing complement-mediated skeletal muscle myoblast lysis. However, the T. cruzi sensitized splenic lymphocytes did produce a lymphokine which was capable of inducing lysis of syngeneic myoblasts by chromium-51 release assay.