01775naa a2200157 a 450000100080000000500110000800800410001910000200006024501720008026000090025252012520026165000160151370000120152970000150154177300610155617854122017-04-06       1981    bl ---       0--  u    #d1 aGASBARRE, L. C.  aMurine T lymphocyte specificity for African trypanosomes. II.Suppression of the lymphocyte proliferative response to Trypanosoma brucei systemic trypanosome infection.  c1981  aPreviously, 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. The exact mechanism of the suppression is not known and appears to function in the absence of demonstrable suppressor cells. Since the cell responses are strictlydependent on the presence of macrophages, we have investigated whether the loss in responsiveness is due to a defect in the T cell populations, or to a loss of macrophage function. Our results shown that T cells taken from mice 3 weeks after priming with T. brucei are unable to mount a profilarative response in the presence of a normal macrophage population and conversely that macrophage taken 3 weeks after infection with T. brucei are unable to elicit a normal proliferative response using a competent primed T cell populations. Thus these results indicate that both populations are affected by the parasite infection.  aTrypanosoma1 aHUG, K.1 aWHO, J. L.  tClinical Experimental Immunologygv.45, p.165-172, 1981.