Murine T lymphocyte specificity for African trypanosomes. II. Suppression of the T lymphocyte proliferative response to Trypanosoma brucei by systemic trypanosome infection.
Previously, we described a system allowing the study of murine T cell-dependent proliferative responses to Trypanosoma brucei antigens. It was observed that T. brucei-specific T cells could be demonstrated in the regional lymph nodes of primed mice for only 2 to 3 weeks following priming. The results of the present study indicate that this inability to demonstrate a long-lived memory response is due to an immunosuppressive effect of the resulting T. brucei infection. The exact mechanism of the suppression is not known, and appears to function in the absence of demonstrable suppressor cells. Since the T cell responses are strictly dependent on the presence of macrophages, we have investigated whether the loss in responsiveness is due to a defect in the T cell population, or to a loss of macrophage function. Our results show that T cells taken from mice 3 weeks after priming with T. brucei are unable to mount a proliferative response in the presence of a normal macrophage population, and conversely that macrophages taken 3 weeks after infection with T. brucei are unable to elicit a normal proliferative response using a competent primed T cell population. Thus these results indicate that both populations are affected by the parasite infection.
D000818:Animals; D001202:Ascitic Fluid / Q000166:cytology; D002455:Cell Division; D005260:Female; D007108:Immune Tolerance; D007114:Immunization; D008264:Macrophages / Q000276:immunology; D008297:Male; D008549:Melarsoprol / Q000627:therapeutic use; D051379:Mice; D013601:T-Lymphocytes / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D014346:Trypanosoma brucei brucei / Q000276:immunology*; D014353:Trypanosomiasis, African / Q000188:drug therapy / Q000276:immunology*
D008549:Melarsoprol