Genetic control of cell-mediated immunity in rats: involvement of RT1.B locus determinants in the proliferative response of T lymphocytes to Listeria antigens.

The cellular requirements for Listeria monocytogenes antigen-induced, specific [3H]thymidine incorporation into lymphoid cells were analysed. Nylon-nonadherent lymph node and peritoneal exudate cells from infected athymic rats and mice failed to respond by proliferation, whereas control cells of thymus-bearing animals gave significant responses. In mice, cells expressing Thy-1 at a high density were required for the initiation of the proliferative response, but cells with lower density also participated in proliferation. Immune T cells alone failed to respond to L. monocytogenes antigen, but the addition of accessory cells provided optimal responses. These were nylon wool adherent, absent from thoracic duct lymph, but present in thymus and lymph nodes and particularly abundant in spleens of nonimmune rats. Accessory cells had to be matched at the B region of RT1, the major histocompatibility complex, to provide a stimulatory signal for L. monocytogenes antigen-specific T cells. Thus, the genetic restriction criteria were the same as for the transfer of delayed-type hypersensitivity to L. monocytogenes antigen, but differed from those controlling the transfer of acquired cellular resistance. The interaction between T cells and accessory cells could be blocked by alloantisera directed against Ia-antigens expressed on the accessory cell population. The study suggests that killed L. monocytogenes bacteria are presented by Ia-positive adherent cells in a RT1.B-restricted fashion to provide a proliferative signal for sensitized T cells.