Some aspects of idiopatyc regulation in Chagas disease and human schistosomiasis

RESUMO

We developed an approach for the examination of antiidiotypic cell-mediated reactivity during chronic human infections. Antibodies against Schistosoma mansoni egg antigens (anti-SEA) and against Trypanosoma cruzi epimastigotes (anti-EPI) prepared from pooled and individual sera from patients with either schistosomiasis mansoni or Chagas disease were immunoaffinity purified on appropriate columns and used to stimulate patients' T cells. These antibodies preparations and their F (ab)2 fragments stimulated in a dose-dependent assay the proliferations of peripheral blood mononuclear cells (PBMC) and T lymphocytes from some, but not all actively infected individuals. Anti-idiotypic T cells can recognize and respond to anti-SEA or anti-EPI idiotypes directly. We contend that the most likely explanation of this stimulations is that the idiotype expressed on these anti-SEA or anti-EPI antibodies are acting as immunogens to stimulate antiidiotypic T lymphocytes that develop during the course of the infection. Immunization of rabbits with these antibodies (anti-SEA or anti-EPI) preparations, followed by absorption of the rabbit antisera on absorbants of normal Ig, produced specific anti-id reagents. Use of these reagents in competitive ELISA distinguished the idiotypic expression on anti-SEA or anti-EPI preparations obtained from patients' sera with different clinical forms of schistosomiasis or Chagas disease, respectively. The anti-SEA Id-reactive T cells from S. mansoni infected patients were capable of regulating autologous in vitro granuloma formation.