Anti-Ly-6E.1-monoclonal-antibody-mediated augmentation of interleukin-2-dependent generation of natural killer cell activity from mouse bone marrow cells.

Studies have shown that the administration of anti-Ly-6E.1 monoclonal antibody (mAb) to tumor-bearing mice augments their T-cell-dependent functional activities, splenic natural killer (NK) cell activity, and antitumor resistance. The effect of the mAb on splenic NK cell activity resembles that of biological-response modifiers, which involves enhanced large granular lymphocyte (LGL) development in the bone marrow (BM) from pre-NK cells, and their subsequent migration and localization in peripheral organs. We analyze here the effect of anti-Ly-6E.1 mAb on the IL-2-dependent generation of NK cell activity in short-term cultures of mouse BM cells. The results indicate that an increase in the population of LGLs paralleled the mAb-mediated augmentation of IL-2-induced generation of NK cell activity in the cultures. Although pre-NK and T cells present in the BM expressed Ly-6 antigens, the augmentation of NK cell generation appears to be due to the mAb interacting with the T cells, not the pre-NK cells, resulting in increased synthesis of tumor necrosis factor-alpha, which in turn enhanced the interleukin-2-dependent development of NK cell activity.