Evidence for Ir Gene Expression in the Antigen-Presenting Cell

Abstract Proliferative responses by peritoneal exudate T-lymphocyteenriched cells (PETLES) from GAT primed mice can be stimulated by GAT-pulsed spleen cells from non-immune animals only if the donors of both cell types are identical at the I-A subregion of the major histocompatibility complex (MHC). However, in 4 separate (high responder × low responder)F1 strains, GAT-primed PETLES could be stimulated by GAT/presenting cells from either the F1 or the high responder parent but not by cells from the low responder parent. Addition of equal numbers of GAT-pulsed low responder spleen cells did not affect the response of F1 PETLES to GAT on high responder spleen cells. Furthermore, pre-treatment of F1 PETLES with anti-Ly 2.2 serum and complement did not allow these cells to respond to GAT-pulsed low responder parental spleen cells. This suggests that the failure of spleen cells from low responder parental strains to present GAT to F1 PETLES is not due to the presence of suppressor cells in either the antigen-presenting or the responding cell populations. These results indicate that control of antigen-presenting cell-T lymphocyte interactions is one site of Ir gene expression.