In the preceding paper we showed that the beige mutation in the mouse leads to a complete impairment in NK cell function, which is predetermined at the level of progenitor cells in the bone marrow. The observations in this report suggest that the beige defect is selective for NK cells since killer function in promonocytes, macrophages, and alloimmune or lectin-generated T cells is relatively normal. In addition, spleen cell-mediated ADCC against chicken erythrocytes and promocyte ADCC against tumor cells was also identical in homozygous mutants or their heterozygous littermate controls. However, spleen cell-mediated ADCC against tumor cells was impaired in bg mice as well as antibody-independent NK cytolysis. When combined with the work of others these results suggest that NK and K cells are identical and one effector can kill by an antibody-dependent or independent mechanism. Since the beige defect lies within the lytic machinery of the cell rather than at the level of target recognition, these results also suggest that the NK lytic mechanism as well as the effector cell type is distinct from that in T cells, macrophages, promonocytes, or nonlymphocytic effectors participating in ADCC. These mice should provide a valuable model for studies of in vivo resistance to tumors, grafts, and virus-infected cells in the absence of functional NK cells.

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This work was supported by the Killam Program of the Canada Council, NCI Contract N01 CB 64023, The Volkswagen Foundation and the German Ministry of Science and Technology, and the Swedish Cancer Society.

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