[Role of homology in the JC subregion of the H2 complex in the reciprocal suppression of normal killer and tumor cells].

Attempts have been made to find out 1/whether there is an interaction between normal killers (NK) and tumor cells transplanted in vivo and how both effectors' cytotoxicity against the third participant - NK-sensitive target cells, is affected by the hypothetical interaction; and 2/the implication of H2-complex in the interaction of both the effectors. Use was made of an experimental three-component model in vitro. It included the effector cells of two types. As NK use was made of splenocytes from C57BL/6; CBA; B10; SM; B10.D2; B10.A(3R); B10.A(5R); BALB/C; A/Sn; B10.D2(R107); B.10.D2(R101) mice. Tumor effectors were EL-4 MX-11 (H2b), L-1210 (H2b) and SA-1(H2b) cells transplanted on syngeneic mice. EL-4 cells adapted in culture in vitro were used as standard target cells. Two types of the effector interaction are described. The homology of NK and tumor effector cells in the D-end of H2-complex in the I-C subregion was found to lead to a marked mutual suppression of both the participants with reference to the third component - EL-4 target cells adapted in vitro. The absence of homology in the DC-end of H2-complex provided an opposite effect - summation of cytotoxicity of NK and tumor effector cells against EL-4 target cells. The authors discuss whether the cause of mutual suppression is repaired cytotoxicity (or membrane toxicity) of NK and tumor cells.