TUMOR-SPECIFIC BOOSTING OF IL-2 INDUCED NK ACTIVATION BY PARAFORMALDEHYDE FIXED TUMOR-CELLS

NK activation in C57B1/6 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 act ivation was carried out in the presence of fixed tumor cells. In addit ion the cytotoxic effector cells generated were resistant to anti-Thy- 1 + C treatment, indicating that the effector cells were not T lymphoc ytes. IL-2 activation of NK cells was compared When fixed YAC or EL4 t umor cells were added during the IL-2 activation phase, it was found t hat the addition of either of these tumor cells significantly boosted the levels of cytotoxic activity generated against both targets. Signi ficantly higher anti-YAC cytotoxic activity was however generated when fixed YAC cells instead of EL4 cells were present during the activati on phase. Similarly, significantly greater cytolytic activity was gene rated against EL4 cells, when fixed EL4 rather than YAC cells were pre sent during the activation phase. Addition of paraformaldehyde fixed s yngeneic or allogenic spleen cells instead of tumor cells, did not boo st 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 cel ls during IL-2 activation phase, may boost the activation of NK cells in a tumor specific manner. (C) 1998 Elsevier Science B.V. All rights reserved.