Mechanisms of the H-2 effect on viral leukemogenesis.
Evidence has been gathered which supports the notion that two distinct but interacting mechanisms, controlled by loci mapping within the H-2 complex, influence Friend murine leukemia virus (FV) disease. One mechanism, controlled by a gene mapping in or close to H-2D, influences the capacity of the H-2D gene product to form molecular complexes with FV molecules in the plasma membrane of infected cells. Formation of a complex appears to provide a target antigen for syngeneic cytotoxic T-lymphocytes, to cause co-capping of FV and H-2D antigens, to permit the selective inclusion of H-2Db molecules into progeny Friend virions, to influence the long-term maintenance of virus production in vitro and, in conjunction with the second mechanism, to stimulate the generation of cytotoxic T-lymphocytes. This second mechanism is controlled by a gene in the H-2K or H-2I region, and, in the presence of an H-2/FV molecular complex immunogen, influences the generation of H-2 restricted cytotxic T-lymphocytes and the rate of rejection of syngeneic FV-induced tumor cells.
D000818:Animals; D000936:Antigen-Antibody Complex; D002462:Cell Membrane / Q000276:immunology; D002874:Chromosome Mapping; D003601:Cytotoxicity Tests, Immunologic; D006649:Histocompatibility Antigens; D009052:Leukemia Virus, Murine; D051379:Mice; D008815:Mice, Inbred Strains; D010950:Plasma Cells / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D014412:Tumor Virus Infections / Q000276:immunology*
D000936:Antigen-Antibody Complex; D006649:Histocompatibility Antigens