Abstract
This review emphasizes some of the differences between the fate of allogeneic H2-incompatible T-cells, when injected into immunodeficient, T-depleted mice, or as parental cells injected into F1 hybrids. In both conditions, allogeneic cells are eliminated, a rejection which cannot be predicted from the fate of a skin graft. While in both situations a phase of GVHR is observed, it is of short duration in allogeneic T-B reactions, and it is obvious that the production of allo-antibodies by the host, which is enhanced by the GVHR, is the major mechanism of allogeneic T-cell elimination, resulting in a rapid self-cure of the GVHR. In T-vs-B GVHR, the enhancement of the humoral response is strikingly restricted to the allo-antigens of the T-cells, and correspond therefore to a peculiar form of "allogeneic effect", in fact an "allogeneic suicide" which implies a linked T-B collaboration, while in P-F1 combinations, there is a enhancement of the humoral response to unrelated antigens (i.e. unlinked T-B collaboration or the classical allogeneic effect) and a polyclonal B-cell activation, which can result from the much more protracted course of the GVHR. The parental cells surviving in the spleen of an F1 semi-allogeneic host, undergoing a lethal GVHR were characterized at the clonal level: they were exclusively of the Lyt 2- MLR responder and polyvalent helper variety. This indicates that the Lyt-2- and polyvalent helper subset is selected during an allo-reaction in vivo (either because it is more rapidly replicating and/or less negatively selected by the host resistance) and that it is capable of inflicting a lethal GVHR.

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