AbstractMice lacking the p56lckmolecule (lck−/−) have a profound block in the maturation of thymocytes and a greatly reduced number of peripheral mature T cells. To analyze further the functions of the T cells developed in lck −/− micein vivo, we evaluated the ability of lck−/− mice to reject allo‐skin grafts and methylcholanthrene (MCA)‐induced syngeneic fibrosarcoma, and also examined the biological activity of lck −/− natural killer (NK) cells. Mice lacking p56lckfailed to reject skin grafts from either MHC‐disparate or minor‐histocompatibility‐different donors, even after they had been primed with donor spleen cells. They also failed to reject the MCA‐induced immunogenic syngeneic fibrosarcoma, MC57X. NK activity in mice lacking p56lckwas normal, and there were no differences in the NK cell activation induced by poly(I) · poly(C) stimulation or interleukin‐2 stimulation (lymphokine‐activated killer induction) between mice lacking p56lckand their immunocompetent heterozygous littermates. NK cells lacking p56lckmediated a normal antibody‐dependent cell‐mediated cytotoxicity (ADCC) response. The results of this study indicate that the loss of p56lckseverely impairs the effectors of the immune system which mediate the rejection of allo‐skin grafts and syngeneic tumors. The normal NK activity in lck −/− mice suggests that p56lckis not required for
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