Chagas, disease, molecular biology, immunology of Trypanosoma cruzi. José Antonio O’Daly Carbonell

Five mitogenic proteins in FCS stimulate T. cruzi division, found in plasma membranes and cytoplasmic granules, changed structure by T. cruzi growth, the base of autoimmunity. An insoluble fraction from T. cruzi membranes lysed cells, it is a lipid, pronase, trypsin, temperature resistant, inhibited by albumin. Inhibition of T. cruzi’s proteolytic activity, key for vaccines’ production. Synthetic medium, allowed T. cruzi growth between 26°- 37°C, with FCS or peptides of glutamic acid, alanine, and lysine. Infected homozygous mice had suppression by macrophages to T and B cell mitogens, parasite antigens, at 17 days postinfection, recovering at chronic phase. Trypomastigotes inhibited response to mitogens, epimastigotes stimulated it, higher than mitogens. Hydroinsoluble protein of 14 -15 kDa, from infected spleens, induced suppression to mitogens thru macrophages. Epimastigotes changed surface proteins, between 30° to 34°C. Lowest parasitemia, longest survival time and no immunosuppression, postimmunization with pellets, from TLCK treated epimastigotes cultured at 30°C. Surface, secreted proteins, T. cruzi extracts have antigens for diagnosis explaining the pathogenesis of Chagas disease.