Interaction antigens detected by cytotoxic T cells with the major histocompatibility complex as modifier

Abstract

THE most exciting aspect of immunology at the moment is the way in which the major histocompatibility complex regulates certain functions of the immune system. Understanding the basis of this will revolutionise our thinking about T cell responsiveness and perhaps explain the puzzling degree of genetic polymorphism of the major histocompatibility complex. Most rewarding also will be the clinical applications, since susceptibility to many diseases is linked to HL-A (refs 1 and 2). Genes which control the response of thymus-derived (T) lymphocytes to certain antigens map in the major histocompatibility complex¹; 1–10% of T lymphocytes respond in an allogeneic mixed lymphocyte culture, or graft-versus-host reaction, against non-self major histocompatibility antigens^3–5; cytotoxic T cells derived from mixed lymphocyte cultures seem to be directed against the classical serologically defined antigens coded in this region^6,7. The work described here derives from another recently reported link between murine T cell function and the major histocompatibility complex. It has now been demonstrated that T-cell mediated lysis of virus infected target cells is restricted by H-2 (refs 8–10). Lysis of TNP modified targets is similarly restricted in another system¹¹. I have now shown that cytotoxic T cells derived from mice immunised with cells from an allogeneic strain which carries the same H-2 region will lyse only targets which share the same H-2 as the immunising strain.