title: Involvement of accessory cells in the Trypanosoma cruzi-induced inhibition of the polyclonal response of T lymphocytes.
abstract: Infection with Trypanosoma cruzi is characterized by hyporesponsiveness of the immune system during the acute phase of infection. To better understand the immunological mechanisms affected by T. cruzi, we studied if a reduced T cell proliferative response could originate from an inability of T cells to proliferate or a functional deficiency at the level of accessory cells (AC). The inhibitory effect exerted by T. cruzi was during the induction phase of the lymphoproliferative response, suggesting the participation of AC in the hyporesponse. Then we further investigated the potential of the parasite to interfere with accessory cell-dependent and -independent pathways of human T cell proliferation. Peripheral blood mononuclear cells and peripheral blood lymphocytes from healthy individuals, enriched for T cells, were analysed with regard to their proliferative capacity using: phytohaemagglutinin, immobilized anti-CD3 monoclonal antibody (MoAb) and MoAb to the CD28 antigen, anti-CD3 MoAb and recombinant IL-2 and anti-CD3 MoAb plus phorbol myristate acetate in the presence of parasites. Significant suppression of the proliferative response was caused by the parasite only when AC were present. The parasite markedly reduced the surface expression of HLA-DR and CD11b antigens, key molecules in PHA-induced proliferation. Addition of indomethacin to the culture failed to reverse the inhibitory effect of the parasites, suggesting that prostaglandin E2 was not involved. These data suggest that AC in contact with T. cruzi become incompetent as antigen presenting cell because they are unable to induce a normal proliferative response in T lymphocytes.
authors.affiliation: Inmunologia Departamento de Bioquimica Clinica, Facultad de Ciencias Quimicas, Universidad Nacional de Cordoba, Argentina.
authors.forename: C
authors.initials: C
authors.lastname: Motrán
authors.forename: A
authors.initials: A
authors.lastname: Gruppi
authors.forename: C M
authors.initials: CM
authors.lastname: Vullo
authors.forename: M C
authors.initials: MC
authors.lastname: Pistoresi-Palencia
authors.forename: H M
authors.initials: HM
authors.lastname: Serra
mesh_terms: D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology*; D002450:Cell Communication / Q000276:immunology; D014355:Chagas Disease / Q000276:immunology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D006684:HLA-DR Antigens / Q000378:metabolism; D006790:Host-Parasite Interactions / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance / Q000187:drug effects; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000187:drug effects; D016177:Macrophage-1 Antigen / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D013601:T-Lymphocytes / Q000276:immunology*; D014349:Trypanosoma cruzi / Q000276:immunology*
chemical_list: D016861:Cyclooxygenase Inhibitors; D006684:HLA-DR Antigens; D016177:Macrophage-1 Antigen; D007213:Indomethacin