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Two experiments are described concerned with the mechanism of host cell activation in the rat popliteal lymph node (LN) undergoing a graft-versus-host (GVH) reaction. (1) Irradiated, F1 hybrid hosts (750 rad) mounted an impaired response to parental strain T cells. This was augmented by an intravenous injection of F1 hybrid lymphocytes but not by parental strain B lymphocytes syngeneic with the initiating T cells. When the donor T cells (footpad) and B lymphocytes (intravenous) were completely allogeneic the residual response of the irradiated F1 was completely inhibited. (2) The popliteal LN response in the semi-allogeneic situation of the type (A x C)F1 leads to (B x C)F1 was, if anything, weaker than in the allogeneic situation AA leads to BB. These results and other data are discussed in terms of a possible major histocompatibility complex (MHC) requirement for host cell activation. The sharing of an MHC haplotype between donor and host cells is unlikely to be a necessary or sufficient condition for host cell activation.
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