Rejection of H-2 class I bm 1 mutant skin allografts by B6 recipient mice is mediated by a population of CD8+anti-bm1 cytotoxic T-lymphocytes that produces and consumes its own T helper factor in response to bm1 skin allografts (dual function CTL).Previously we have demonstrated that transfusion of allogeneic lymphocytes across an H‐2 class I disparity induces specific long‐lasting skin allograft survival.We now show that intravenous injection of allogeneic spleen cells across the bml mutant disparity results in a temporary decrease of donor‐reactive CTLp in the spleen of recipient mice, lasting for approximately five weeks. The sponge matrix allograft model was used to show that allograft tolerance is caused by a specific functional clonal deletion of CTLp within the allograft. We propose that dual function CTL are vetoed by donor T cells, resulting in skin allograft tolerance.