Antiheart antibody-dependent cytotoxicity in the sera of mice chronically infected with Trypanosoma cruzi

Abstract

Sera of mice chronically infected with Trypanosoma cruzi contain antibodies that bind to the surface of living adult syngeneic heart muscle cells. In a syngeneic system, with nonadherent spleen mononuclear cells as effector cells and cardiocytes as targets, antibody-dependent cytotoxicity (ADCC), revealed by the liberation of creatine phosphokinase from damaged cardiocytes, was observed after incorporation of serum samples from infected mice. Target damage was decreased after absorption with syngeneic myocardium, but absorption with T. cruzi epimastigotes or trypomastigotes or with syngeneic skeletal muscle had no effect on ADCC. No complement-dependent lysis against heart muscle cells was detected in the same serum samples. These observations indicate that serum from chronically chagasic mice contain antibodies that bind to the surface of living adult syngeneic cardiocytes and are able to exert ADCC, suggesting that they could play a role in the pathogenesis of the heart damage that occurs in Chagas' disease.

Major Trypanosoma cruzi antigenic determinant in Chagas' heart disease shares homology with the systemic lupus erythematosus ribosomal P protein epitope

“…Serum samples were diluted 1:1,000, incubated with increasing concentrations of conjugated peptide R-13 (O), R-10 (A), R-7 (O), or AEAELVKMALMKV (@), and assayed for binding to JL5 fusion protein. 16,19,23), may operate alone or in association and may contribute to generate the chagasic anti-P response.…”

Characterization of the recognition specificity of autoreactive, polyspecific monoclonal antibodies obtained from spleen cells of parasite‐infected BALB/c mice

“…Numerous reports demonstrated the presence of autoantibodies in parasite-infected hosts. In some studies, it has been shown that autoantibodies found in parasite-infected hosts recognize not only normal tissue but the infected parasite itself (Khoury et al 1979, Szarfman et al 1982, Said et al 1985, Laguens, Meckert & Chambo 1988, Van Voorhis & Eisen 1989, Ternynck et al 1990, Ternynck et al 1991). However, it was not known whether these autoantibodies recognize antigenic determinants cross-reactive with autologous or heterologous parasite antigens such as demonstrated in this study.…”

“…1991). On the other hand, autoantibodies cross reactive with parasites have been reported with T. cruzi (Szarfman et al 1982, Snary et al 1983, Said et al 1985, Laguens, Meckert & Chambo 1988, Van Voorhis & Eisen 1989. These phenomena are interesting in two respects.…”

“…First, as suggested in work with T. cruzi , Szarfman e6 al. 1982, Snary et al 1983, Said et al 1985, Laguens, Meckert & Chambo 1988, Van Voorhis & Eisen 1989) these autoantibodies may be causative agents for pathogenesis of parasite infection. Secondly, this may be a protective mechanism against host attack; parasites mimic host molecules thereby avoiding the host immune response.…”

Presence of parasite antigen on the surface of P388D1 cells infected with Ehrlichia risticii

“…Antibodies directed at parasite antigens are known to induce the lysis of cells infected with various viruses (11,14,28), Coxiella sp. (17), and protozoa (18,22,27) by the action of antibody and complement and/or antibody-dependent cellular cytotoxicity (ADCC). Despite binding to infected cells, however, antibodies to chlamydial genus-specific lipopolysaccharide antigen on the surface did not induce complement-mediated cytolysis (15), and ADCC was not examined.…”