New alloantigen genetically linked to the major histocompatibility locus of the mouse

Abstract

THE mouse H-2 locus and its genetic homologue, the HL-A locus in man, are much more complex than originally envisaged, and are now referred to as the major histocompatibility complex (MHC)¹. Transplant rejection is more closely correlated with mixed lymphocyte reaction (MLR) than with tissue typing^2–6 and in addition to an MLR region in the MHC other regions are of obvious importance in the context of recognition, for example the immune responsiveness regions (Ir)^7,8. The only gene products of the MHC so far characterised are those recognised serologically by ‘tissue typing’ antisera, that is, H-2 antigens and their homologues in other species. These products are not the only substances involved in the fate of allografts; indeed sensitisation against an allograft seems to require MLR differences although serologically detected components have an, as yet undefined, role in the effector arc of rejection^9–11. Though there are suggestions that MHC gene products other than H-2 (HL-A, and so on) may be primarily involved in graft rejection¹², the only in vivo studies pointing strongly in that direction were carried out in the rat enhancement model¹³. In these studies rat heart allografts were passively enhanced by alloantisera from which Ag-B (the H-2 homologue in rats) antibodies had been removed by absorption with appropriate red blood cells (RBC), which suggests a role for antibodies directed against other products of the MHC.