The ready availability of inbred strains, ability to withstand microvascular surgery, and the ease of production of immunological enhancement have made the rat a popular and valuable model for organ transplantation. A number of studies in the mouse employing skin allografts have demonstrated the central role of gene products of the major histocompatibility H-2 complex in the rejection process. Fragmentary understanding of the rat major histocompatibility gene complex (MHC) 1 has limited the general applicability of data obtained by studying rat organ transplantation. Because important differences exist between the immunobiology of skin and organ allografts (1), it is important to develop a full understanding of the rat MHC. Recent studies have indicated that rat gene products identical to or closely linked to the serologically defined Ag-B system function as immune response genes (2, 3) and stimulate the mixed lymphocyte culture response (4). These studies suggest, therefore, that the rat MHC bears close similarity to the more extensively mapped MHC regions of primates and the mouse.The phenomenon of passive enhancement of tumor and tissue allografts (1, 5) has been shown to be associated with only minimal alteration in cellular immune responsiveness in the host (6). In contrast, immunopathological (7,8) and humoral studies (6-9) have emphasized the depression of host humoral responsiveness and suggest an impairment of B-T-cell cooperation (6). Still, the mechanism by which passive immunization produces this deviation in the immune response remains speculative. An important recent advance has been the finding that, while antibodies of different classes (10) and physicochemical characteristics (11) can induce enhanced graft survival, antibodies specific for the products of the K and D regions of the mouse MHC are unnecessary (12). Similarly, in the rat,