A receptors induced

We have previously shown that lymphoblasts al- loactivated in vitro acquire the capacity of stimulating the autolo- gous mixed lymphocyte response. This response is anti-idiotypic in nature because lymphocytes so primed display accelerated memory responses' only when restimulated by autologous lym- phoblasts that have been alloactivated against the same.HLA-DR antigen. Based on this observation we have postulated that the absence of HLA antibodies in alloimmunized human subjects may be due to.the development of autoantibodies that react with the anti-HLA receptors expressed by primed lymphocytes or by anti- HLA antibodies or both. This hypothesis has been confirmedwin the present investigations which show that sera from parous women react with autologous T lymphoblasts primed in 5-day mixed lymphocyte culture against their husband-i.e., with lym- phoblasts expressing receptors for the immunizing donor. Anti- HLA receptors expressed by T and B lymphocytes seem to share serologic determinants because sera that bind to autologous al- loactivated lymphoblasts are also capable of inhibiting the anti- HLA activity of autologous and homologous sera. Auto-anti-idi- otypic antibodies inhibit the autologous mixed lymphocyte re- sponse, to autologous alloactivated lymphoblasts, a phenomenon whose in vivo correlate may reside in autoinhibition of anti-HLA antibody formation and of allograft immunity. Because auto-anti- idiotypic antibodies were found in sera from all parous women tested, the hypothesis that nonresponsiveness to alloantigens exists as a state per se is not likely. The passive transfer of antireceptor (idiotype) immunity by use of antibodies from pregnant women's sera may provide a powerful tool for specific suppression of al- lograft rejection.