Genetic Restrictions for the Induction

Gene products of the major histocompatibility complex (MHC) 1 are associated with various effector and cooperative functions of immunocompetent lymphoid cells (1). The I region of the MHC is associated with the induction of helper T cells (2), the proliferative response of T cells to allogeneic cells (3) and to antigen-pulsed macrophages (4), cooperation of T helper cells with B cells (5), and the adoptive transfer of delayed-type hypersensitivity (DTH) to fowl gamma globulin (6). Gene products of the H-2K and/or H-2D regions of the MHC are associated with T-cell-mediated cytolysis of virus-infected (7) or hapten-modified (8) target cells, and the~transfer of DTH to murine lymphocytic choriomeningitis virus (9). We have recently been studying the induction and mechanisms of haptenspecific T-cell tolerance to 1-fluoro-2,4-dinitrobenzene (DNFB) contact sensitivity by using dinitrophenyl (DNP)-modified lymphoid cells (DNP-LC) as tolerogens (10). Tolerance induced by DNP-LC has been functionally separated into two mechanisms-clone inhibition and the participation of suppressor T cells (Ts) (11). We have also reported that the induction of Ts by DNP-syngeneic LC (syninduced Ts) (12) as well as the expression of Ts induced by DNP-allogeneic LC (alloinduced Ts) (13) is genetically restricted by MHC gene products. In the present report, we have investigated these genetic restrictions by using congenic resistant mouse strains. The results indicate that both syninduced and aUoinduced Ts are activated by hapten-modified determinants coded for by the H-2D region of the MHC. Furthermore, the results show that alloinduced Ts are