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Abstract

The protozoan Trypanosoma cruzi, is the causative agent of Chagas disease, which is endemic in many Latin American countries. The finding of a T cell-rich inflamatory mononuclear cell infiltrate in the presence of extremely few parasites in tissue lesions can doubt on the direct participation of T. cruzi in the pathogenic mechanism, and suggested the posible involvement of autoimmunity. Such an anti-tissue autoimmune response could be triggered either by molecular mimicry with some parasite antigens homologous to tissue proteins, or by the display of intracellular sequestred tissue proteins. Antibodies to T. cruzi have been found to cross-react with host components, and T cells directed against cardiac and nervous sistem have been found in mice with experimental Chagas disease. T cells directed against T. cruzi antigens which crossreact with nervuos tissue have been found to recreate nervous tissue pathology when transferred to naive animals. These features suggest to the hypothesis of an autoimmune process leading to chronic disease where T. cruzi antigenically mimics host tissues. In order to investigate whether amastigote specific recombinant protein induces antibodies that cross-react with host components, the DNA insert of an amastigote specific cDNA clone (Am230), was subcloned in an expression vector and fusion protein (pMAL-Am230) purified by affinity chromatography. Polyclonal antibodies against pMAL-Am230 localizes the native protein (66 kDa) on the surface's parasite, and cross-react with a cardiac tissue protein of 97 kDa. By tissue immunoperoxidase staining tha anti-pMAL-Am230 antibodies reacted with miocardics fibers. The above results suggest that the 66 kDa amastigote specific protein could be a candidate antigen for autoimmune mimicry leading to cardiac tissue pathology.