Abstract
Protein A (pA), was found to augment the natural killing (NK) activity of peripheral blood lymphocytes against Burkitt's lymphoma‐derived Raji and Daudi cells. This pA‐enhanced NK activity was determined using the ^51^Chromium release microcytotoxicity assay. It was found that the increased NK activitiy was dependent on the concentration of pA used. In addition, the pA‐enhanced NK activity was dependent on the time of incubation of pA with the effector and target cell mixture. Pretreatment of effectors for 16 h or more dramatically increased the NK activity against a wide range of tumor targets of different origin and possessing either B, T or null cell surface characteristics. The presence of the Epstein‐Barr virus (EBV)‐genome in the target cells did not influence the pA‐enhanced NK activity. Nylon‐wool column‐fractionated, non‐adherant lymphocytes (enriched in NK cells) showed an increased NK activity in the presence of pA than unfractionated lymphocytes. Pretreatment of certain targets with pA rendered them more sensitive to NK lysis. Interferon production was readily detected in supernatants from cultures of pA‐treated effectors or effector‐target mixtures, but not in supernatants from pA‐treated target cultures tested. Results of different physicochemical treatments indicate that the pA‐induced interferon is of γ type (type II). Thus, the data presented suggest that the pA‐induced enhancement of NK activity is most likely mediated by the pA‐induced interferon.