Natural killer and T-cell potentiation by monoclonal IgG against natural killer cell FcR(IgG) or the T3 complex.

Treatment of human natural killer (NK) cells with monoclonal antibodies of the IgG isotype against NK cell-FcR(IgG) increased lysis of most haematopoietic target cell lines with high or intermediate background NK susceptibility. Treatment of normal non-adherent lymphocytes with an IgG anti-T3 monoclonal antibody also increased lysis against the same target cells. Potentiating anti-FcR antibodies rapidly modulated FcR activity and the capacity of the cells to act as antibody-dependent killers, although such antibodies were demonstrable for a long time at the cell surface. Anti-FcR treatment did not influence concanavalin A (Con A)-dependent killing, in contrast to anti-T3 treatment, which suppressed lectin-dependent lysis but did not influence antibody-dependent killing. The data is compatible with a 'pro-receptor' theory for FcR in NK killing, stating that such receptors may function in the same way as the T3 complex interacts with specific T cell receptors.