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Skin graft enhancement studies with antigenic differences arising from the H-2K, H-2D, and H-2L loci
Enhancement of skin grafts was previously shown to be possible when there were antigenic differences arising from the @K end" but not the @D end" of the H-2 complex. Subsequent studies demonstrated that anti-Ia antibodies in the anti-K end sera were responsible for graft prolongation and not the anti-H-2K antibodies and that D end antisera were not enhancing as they lacked Ia antibody activity. The studies reported herein have extended these findings by two separate approaches. First, by using appropriate congenic and recombinant strains, enhancement by D end antigenic differences could be observed, provided that Ia antibodies were also present. In this way, H-2D and H-2K alloantigens are similar and both require additional I region differences to enable skin graft enhancement to be observed. Second, H-2Kb, H-2Dd, and H-2Ld mutants were examined and putative antisera used to attempt to prolong graft survival in these unique coisogenic strains. In no case was graft survival significantly prolonged, even in the presence of demonstrable antibodies. Therefore, in two different approaches, wherein single gene products were examined (derived by mutation and by recombination), enhancement of skin allografts could not be observed, unless additional Ia alloantigenic differences were also present.
Enhancement of skin grafts was previously shown to be possible when there were antigenic differences arising from the @K end" but not the @D end" of the H-2 complex. Subsequent studies demonstrated that anti-Ia antibodies in the anti-K end sera were responsible for graft prolongation and not the anti-H-2K antibodies and that D end antisera were not enhancing as they lacked Ia antibody activity. The studies reported herein have extended these findings by two separate approaches. First, by using appropriate congenic and recombinant strains, enhancement by D end antigenic differences could be observed, provided that Ia antibodies were also present. In this way, H-2D and H-2K alloantigens are similar and both require additional I region differences to enable skin graft enhancement to be observed. Second, H-2Kb, H-2Dd, and H-2Ld mutants were examined and putative antisera used to attempt to prolong graft survival in these unique coisogenic strains. In no case was graft survival significantly prolonged, even in the presence of demonstrable antibodies. Therefore, in two different approaches, wherein single gene products were examined (derived by mutation and by recombination), enhancement of skin allografts could not be observed, unless additional Ia alloantigenic differences were also present.