Tumor specific boosting of IL-2 induced NK activation by paraformaldehyde fixed tumor cells

Abstract

NK activation in C57Bl/6 mouse spleen cells was carried out with IL-2 in the presence or absence of paraformaldehyde fixed YAC tumor cells. Generation of anti-YAC cytolytic activity was markedly higher when activation was carried out in the presence of fixed tumor cells. In addition the cytotoxic effector cells generated were resistant to anti-Thy-1+C treatment, indicating that the effector cells were not T lymphocytes. IL-2 activation of NK cells was compared When fixed YAC or EL4 tumor cells were added during the IL-2 activation phase, it was found that the addition of either of these tumor cells significantly boosted the levels of cytotoxic activity generated against both targets. Significantly higher anti-YAC cytotoxic activity was however generated when fixed YAC cells instead of EL4 cells were present during the activation phase. Similarly, significantly greater cytolytic activity was generated against EL4 cells, when fixed EL4 rather than YAC cells were present during the activation phase. Addition of paraformaldehyde fixed syngeneic or allogenic spleen cells instead of tumor cells, did not boost NK activation in response to IL-2, indicating that the boosting of NK activation did not result from exposure to alloantigens during the activation phase. These results indicate that an exposure to tumor cells during IL-2 activation phase, may boost the activation of NK cells in a tumor specific manner.