DISTINCT ALLOANTIGENS TRIGGER PROLIFERATIVE OR NONPROLIFERATIVE T LYMPHOCYTE ACTIVATION IN CBA/N, CBA/J, AND C3H MICE

Abstract

Lymphokine release and proliferation take place during 1-way murine mixed leukocyte culture (MLC) when responder and stimulator cells differ in H-2 alloantigens; a dissociation of these 2 functions can be observed where there are incompatibilities in non-H-2 alloantigens. It is possible that this dissociation depends on different thresholds of activation of the 2 responses, or that some non-H-2 alloantigens selectively activate lymphokine release or proliferation. To investigate this question, H-2-matched CBA/N, CBA/J, C3H/HN, (CBA/N .times. CBA/J)F1 and (CBA/N .times. C3H/HN)F1 leukocytes were used, both as responder and stimulator cells. CBA/N mice and the male F1 hybrids obtained from CBA/N mothers carry an X-linked immune defect that results in an arrest of B lymphocyte maturation. In the majority of MLC combinations tested, migration inhibition factor (MAF) release and proliferation took place in parallel. CBA/N, but not F1 leukocytes, stimulated MIF release and not proliferation by CBA/J responders; C3H/HN leukocytes stimulated proliferative responses but not MIF release by CBA/N responders. Since proliferation and MIF release have a similar threshold of activation, their dissociation indicates that different non-H-2 alloantigens can specifically activate distinct T cell functions. Previously unsuspected alloantigen differences between CBA/N and CBA/J are revealed by MIF release.