Hybrid resistance in vitro. Possible role of both class I MHC and self peptides in determining the level of target cell sensitivity.

摘要: NK cells of F1 hybrids frequently exhibit an enhanced capacity to reject semisyngeneic parental bone marrow grafts, a phenomenon known as hybrid resistance. Attempts define the mechanism whereby this occurs have been hampered by factors inherent in use vivo model, including host immune response, microenvironment, cell trafficking patterns, and irradiation. We show here that IL-2-activated (lymphokine-activated killer cells) can be used establish vitro model appears mimic These effectors lyse lymphoblast targets pattern consistent with observed vivo, bear not T surface markers, recognize target structures mapping MHC. By using we then demonstrate sensitivity lysis syngeneic lymphoblasts augmented exposing conditions reported permit exchange endogenous class I-bound self peptides for exogenous foreign sequences. data suggest both MHC I molecules "self" they bind contribute determining susceptibility resistance, are discussed context recognition which is mediated complex molecule it samples from intracellular peptide pool.