Five mitogenic proteins in FCS stimulate the division of T. cruzi, which can be found in plasma membranes and cytoplasmic granules. Their structure is altered by the growth of T. cruzi and forms the basis of autoimmunity. The insoluble fraction from T. cruzi membranes lyses cells, is a lipid, temperature-resistant, and is inhibited by albumin. Inhibiting the proteolytic activity of T. cruzi is key to vaccine development. A synthetic medium allows the growth of T. cruzi between 26° and 37°C, using FCS or peptides of glutamic acid, alanine, and lysine. In infected homozygous mice, there was suppression of T- and B-cell mitogens as well as parasite antigens by macrophages 17 days post-infection, which recovered in the chronic phase. Trypomastigotes inhibited the response to mitogens, while epimastigotes stimulated it more than mitogens. A water-soluble protein of 14-15 kDa from infected spleen induced the suppression of mitogens by macrophages. Epimastigotes altered surface proteins between 30° and 34°C. The lowest parasitemia, longest survival time, and no immune suppression occurred after immunization with pellets of TLCK-treated epimastigotes cultured at 30°C. Surface proteins, secreted proteins, and T. cruzi extracts contain antigens for diagnosis that explain the pathogenesis of Chagas disease.