INHIBITION OF ANTIGEN-INDUCED PROLIFERATION OF T-CELLS FROM RADIATION-INDUCED BONE-MARROW CHIMERAS BY A MONOCLONAL-ANTIBODY DIRECTED AGAINST AN IA DETERMINANT ON THE ANTIGEN-PRESENTING CELL

Chimeric B10.A T cells that had matured in a (B10.A .times. B10.Q)F1 [mouse] environment acquired the ability to respond to poly(Glu56Lys35Phe9) (GL.vphi.), an antigen to which the B10.A mouse is a nonresponder. The response of the chimeric B10.A T cells was initiated by GL.vphi. on responder B10.Q antigen-presenting cells (APC) but not by GL.vphi. on nonresponder B10.A APC. Similarly, chimeric B10.Q T cells that had matured in a (B10.A .times. B10.Q)F1 environment acquired the ability to respond to poly(Glu60Ala30Tyr10) (GAT) when the antigen was presented on responder B10.A APC, but not when GAT was presented on nonresponder B10.Q APC. No syngeneic haplotype preference was observed for either antigen. These interactions between H-2 nonidentical T cells and APC were inhibited by anti-H-2 antisera and a monoclonal anti-Ia antibody directed against the APC but not by such antibodies when they were directed against the T cell. When they develop in a responder chimeric environment, genotypic nonresponder T cells probably become rsponders by acquiring receptors that allow them to recognize responder I region products on the surface of APC. The site of action of the blocking effects of the anti-Ia antibodies apparently is the APC, thus providing strong evidence in support of the idea that Ia antigens on APC are the Ir gene products.