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Mechanisms of the H‐2 Effect on Viral Leukemogenesis
Author(s) -
BUBBERS J. E.,
BLANK K. J.,
FREEDMAN H. A.,
LILLY F.
Publication year - 1977
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1977.tb02117.x
Subject(s) - immunogen , cytotoxic t cell , in vitro , biology , gene , antigen , gene product , virus , cytotoxicity , microbiology and biotechnology , chemistry , virology , genetics , gene expression , antibody , monoclonal antibody
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‐2D b 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 cytotoxic T‐lymphocytes and the rate of rejection of syngeneic FV‐induced tumor cells.