Trypanosoma cruzi Antibodies in Mice Infected with Different Strains of T. cruzi

Peralta, José Mauro; Filardi, Leny S.; Loures, M. A.; Torres, Silvio T.

doi:10.2307/3280832

Cited by 5 publications

(1 citation statement)

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“…The study presented here, with a mouse strain relatively resistant to T. cruzi, showed compromised cardiac tissue with sparse nests of amastigote forms 3 months after infection, which indicated evolution to the chronic phase. Specific IgG antibody response to the Y strain of parasites was high compared with previous results with either the same parasite strain and a B10 congenic mouse strain (19) or the same mouse strain but the Peruana, 21SF, and Colombiana strains of T. cruzi (2). A significant DTH response to parasite antigens indicated that mice were able to build a specific cellular immune response that persisted in the chronic phase, overcoming the immunosuppression that takes place during the onset of the disease (4).…”

Section: Discussioncontrasting

confidence: 38%

Immunopathology of experimental Chagas' disease: binding of T cells to Trypanosoma cruzi-infected heart tissue

et al. 1990

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The immunopathology of Chagas' disease was studied in the experimental model of chronic infection in C57BL/10JT or mice. Sublethal infection with Trypanosoma cruzi, Y strain, induced specific antibodies and a delayed hypersensitivity response to parasite antigens. Mice developed chronic chagasic myocarditis but not skeletal muscle myositis. Binding of T cells to infected heart tissue was investigated during short-term cocultivation of lymphocytes with heart cryostat sections. T cells from infected mice and from normal controls bound equally to myocardium and liver sections from both infected and normal mice. A search in depth was attempted with cells heavily tagged with 99mTc. Labeled T cells from chagasic mice bound to both normal and infected myocardium slices. 99mTc-labeled T cells from controls gave the same binding values. Glass-adherent spleen cells behaved identically to T cells. Prior treatment of the tissue with serum from chronically infected mice did not increase the number of binding cells. Peritoneal macrophages tagged with 99mTc-sulfur colloid also bound to infected myocardium slices. The binding of macrophages was not changed by pretreatment of infected tissue with anti-T, cruzi antibodies. In short, this work did not detect any population of T cells or macrophages which could bind specifically to infected heart tissue to initiate an autoreactive process.

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Section: Discussioncontrasting

confidence: 38%