The major histocompatibility complex (MHC) of the rat, RT1, controls immunological reactions that are analogous to those observed in the mouse, but the molecules encoded by R T1 do not display the degree of polymorphism seen in the mouse H-2 system (Cramer et al. 1978). Because extensive polymorphism of MHC alleles might be related to the primary function of these molecules, we have developed and carefully characterized a congenic rat strain (DA. 1GV 1) with a wildderived haplotype on the DA background (the strains used in these studies are listed in the legend to Figure 1). Previous results (D. L. Gasser, B. A. Winters, and D. V. Cramer, unpublished observations) suggested that the wild-derived haplotype was similar to the inbred R T1 g haplotype. We now describe how this haplotype differs from the original RT1 Β° haplotype and the usefulness of this variant haplotype (RT1 ~'1) in analyzing the CT alloantigenic system.
Ear skin from l l DA.1GVt donor rats was grafted onto the lateral thoracic walls of 11 (DA x KGH)F1 hosts; all 11 grafts were rejected with survival times ranging from 17-48 days. Syngeneic grafts within these two strains survived for over 100 days, the criterion for acceptance. To confirm that rejection was attributable to an MHC-linked difference, ear skin from ten DA x (DA x DA.1GV1)Ft rats was grafted onto (DA x KGH)F1 recipients. The donor animals were MHC-typed with both the mixed lymphocyte reaction (MLR) assay and the class II-specific monoclonal antibody, H76 (Gasser et al. 1979), which cross-reacts with DA.1GV1 but not DA cells. Grafts from all six RTlaV~/RT1 Β°~1 heterozygous donors were rejected (16-64 days) while grafts from the four RTIa~I/RTla~I homozygotes survived.
Three different methods were employed to characterize and identify the molecule(s) causing graft rejection. In the primary MLR, KGH and DA.1GV1 cells were unable to stimulate one another (Table 1), suggesting that these two strains are