PHYSIOLOGICAL INTERACTION DOES NOT EXPLAIN H-2 REQUIREMENT FOR RECOGNITION OF VIRUS-INFECTED CELLS BY CYTOTOXIC T-CELLS

B10.A (H-2Kk, H-2Dd) ectromelia-immune T [thymus-derived] cells from secondary responses in vitro were potent killers of infected [mouse fibroblast] L929 (H-2Kk, H-2Dk) and infected [mouse mastocytoma] P-815 (H-2Kd, H-2Dd) target cells. Specific competition with unlabeled targets showed that 2 separate T cell subsets were responsible for lysis of infected L929 and infected P-815 cells. T cells which kill 1 target (e.g., infected L929 cells) apparently display only 1 out of 2 possible self-complementary recognition structures, in this example the H-2Kk alloantigen, not H-2Dd, whereas T cells that lyse infected P-815 targets display only H-2Dd, not H-2Kk. This hypothesis was tested and seems untenable because of the following results: A.TH (H-2Ks, H-2Dd) ectromelia-immune, secondary cytotoxic T cells which killed infected SJL/J (H-2Ks, H-2Ds) targets were themselves inactivated by pre-incubation with SJL/J cytotoxic T cells generated in a 1-way mixed lymphocyte reaction (MLR) against BALB/c (H-2Kd, H-2Dd). A.TL (H-2Ks, H-2Dd) ectromelia-immune secondary cytotoxic T cells which killed infected BALB/c targets were themselves inactivated by BALB/c cytotoxic T cells generated in MLR against SJL/J. Virus-immune T cells which lyse infected targets by virtue of shared H-2K display H-2D alloantigen, and vice versa.