The role of the host immune response in the development of tissue lesions associated with African trypanosomiasis in mice.

A variety of tissue lesions occurs in African trypanosomiasis, in the pathogenesis of which direct toxic effects of the parasite as well as immunological mechanisms may be involved. The purpose of the present study was to evaluate the role of the host immune response in inducing tissue damage in this disease and particularly in the production of lesions in striated muscle. The development of muscle lesions in T. brucei infection was studied in several groups of mice with different forms of immunodeficiency, as well as in normal mice. In the normal mice, foci of intense inflammation and necrosis were found in the cardiac and skeletal muscles 2 weeks or more after infection. In these lesions, there was a heavy deposition of IgG and IgM, and of trypanosomal antigens. In irradiated, newborn mice, and athymic nude mice infected with T. brucei, these inflammatory lesions were not found, although large numbers of trypanosomes were present between the muscle fibres. The characteristic lesions could be induced in athymic nude mice by transfer of normal spleen cells or of normal T lymphocytes 1 week after the onset of infection. The lesions were also partly induced by transfer of antibody to T. brucei. No antibodies to tissue components, particularly to cardiac myofibrils, were found in any of the infected mice. The results of this study show that immunodeficiency suppresses the development of the characteristic muscle lesions of African trypanosomiasis. The relative importance of humoral and cellular immune mechanisms in the pathogenesis of these lesions is not year clear.