VIRUS-MEDIATED INDUCTION IN HUMAN-LYMPHOCYTES OF ANTIBODY-INDEPENDENT CYTO-TOXICITY (VDCC) AND ENHANCEMENT OF ANTIBODY-DEPENDENT CYTO-TOXICITY (ADCC) AGAINST NATURAL KILLER-RESISTANT TUMOR TARGET-CELLS

The effect of Parotis virus on the in vitro cytotoxicity of human lymphocytes against NK[natural killer]-resistant mouse mastocytoma cells was studied. In the 51Cr-release assay, treatment of lymphocytes with virus induced a rapid cytotoxicity in the absence of anti-P815 antibody (virus-dependent cellular cytotoxicity, VDCC) and strongly enhanced antibody-dependent cytotoxicity (ADCC). At the effector cell level, virus treatment increased the frequency of target-binding cells (TBC) as well as the proportion thereof mediating VDCC and/or ADCC, indicating recruitment of active effector cells. The recruited cells were heterogeneous but contained a major fraction bearing the T-cell-associated antigen T3. Virus decreased rather than increased the recycling capacity of the cytotoxic lymphocytes, suggesting that VDCC induction and ADCC enhancement were due to a virus-mediated improvement of effector cell-target cell interactions. VDCC and ADCC enhancement may be of protective importance in early phases of virus infection as well as for the production of nonspecific tissue injuries associated with viral disease.