H - 2 - Linked Dominant Genetic Control of Immune Suppression by the Random

In the companion paper, the random copolymer of L-glutamic acids°-L-tyrosine" (GTf was shown to be unable to stimulate the formation of specific antibodies in 19 inbred and congenic resistant strains of mice (1). In several of these strains, however, GT complexed to methylated bovine serum albumin (GT-MBSA) was able to stimulate specific plaque-forming cell (PFC) responses . Furthermore, immunization with GT as early as 3 days and as late as 28 days before GT-MBSA was able to suppress a primary response to GT-MBSA in BALB/c mice . Unresponsiveness to GT-MBSA could be transferred to normal, syngeneic recipients with spleen cells or thymocytes from GT-primed BALB/c mice, demonstrating that GT is able to stimulate the development of suppressor cells in this strain of mouse. In the present study, we have investigated whether GT preimmunization could inhibit the response to GT-MBSA in several inbred strains as well as congenic resistant strains of mice . Some strains of mice behave like BALB/c mice in this respect, whereas in other strains ofmice, GT preimmunization does not have a tolerogenic effect on the response to GT-MBSA . The development of GT-specific unresponsiveness is inherited as adominant trait. The development of specific immune suppression in response to GT immunization will be shown to be controlled by a gene or genes in the H-2 major histocompatibility complex. In other experiments, we compared the specificity of the suppression induced by GT and by the copolymer of L-glutamic acide°-L-alanine 3°-L-tyrosine'° (GAT) on the response to these copolymers complexed with MBSA by mice bearing the nonresponder haplotypes H-2q and H-2 ,1 .