Anti-viral cytotoxic T cells (Tc) recognize virus only in conjunction with class I MHC molecules in man and mouse (Zinkernagel and Doherty 1979). Antibodies directed to the target cell H-2 molecule inhibit T-cell-mediated cytotoxicity, while no inhibition is observed when anti-H-2 binds to the Tc and not the target (Braciale et al. 1982, Albert et al. 1982). When a series of monoclonal antibodies (mAbs) binding to the same H-2 molecule are used for this type of experiment, differential blocking can be demonstrated in a given virus system or between various virus or minor H antigen systems. For example, antibody H100-27 (antibody 27), which reacts with the D k molecule, was shown to inhibit male-specific cytotoxicity restricted to H-2Dk, but did not interfere with D k allogeneic killing nor with H-2D krestricted cytotoxicity specific for minor H antigens (Lindahl and Lemke 1979). The same mAb blocked cytotoxicity by Tc cells specific for H-2D k and influenza virus but not bebaru-virus-infected O k target cells (Blanden et al. 1979). In CBA/Ca mice, influenza-specific Tc were inhibited by antibody H100-30 (antibody 30) but not by antibody H100-5 (antibody 5, Askonas and Webster 1980), two mAbs known to react with distinct clusters of determinants on H-2K k (Lemke and H~immerling 1982). Similarly the lysis by clones of Tc cells of allogeneic (Weyand et al. 1981) or of influenza-virus-infected target cells (Braciale et al. 1982) can be differentially inhibited by H-2-specific mAbs.
Because mAbs to distinct determinants on H-2 appeared to exhibit such specificity in their blocking action, even if they do not necessarily detect the T-cell restriction site, we chose this approach to study recognition of H-2K molecules by influenza-specific Tc generated in a series of six H-2 k mouse strains following influenza infection.
Five mAbs binding to different clusters of determinants on K k molecules were tested for their effect on influenza-specific Tc lysis. Antibodies 5, 30 and 27 react with determinants m3, m5 and m4, respectively, and antibodies 5 and 30 do not block each other's binding and therefore are in distinct determinant clusters (Lemke and H~immerling 1982). 11-4.1 (Oi et al. 1979) has not been mapped and 16-3-22s (Ozato et al. 1980) is directed to a private K k specificity.