The H-2 complex regulates both the susceptibility to mouse viral lymphomagenesis and the phenotype of the virus-induced lymphomas.
Neonatal infection of C57BL/10 mice with cloned ecotropic and/or dualtropic mink cell focus-inducing (MCF) mouse leukaemia viruses (MuLV), induces a wide spectrum of different lymphomas of T, B, and non-T/non-B cell types. The H-2 complex has a marked influence on both the development of lymphoma incidence and lymphoma type. A study using the oncogenic MCF 1233 virus and a series of B10 congenic mice enabled the mapping of the following: Resistance to the early development of T cell lymphoma is controlled by the H-2I-A locus. Susceptibility to early T cell lymphomagenesis is associated with an I-A-regulated low anti-MCF 1233 envelope antibody response and persistent infection of the thymus. B10 (H-2b) mice, which are resistant to early T cell lymphomagenesis induced by MCF 1233 or other MuLV isolates, have high anti-MuLV envelope antibody responses which are I-A-regulated. These mice develop more B cell lymphomas late in life in contrast to the early development of T cell lymphoma in B10.A (H-2a) mice. The possible response mechanisms which underlie these observations, including: I-A-regulated immunoselection against MuLV antigens expressed by (pre) leukaemic T cells, aberrant expression of class II MHC antigens on some B cell lymphomas and I-A-regulated chronic immunostimulation of MuLV-expressing (pre) leukaemic B cells, are discussed.
D000818:Animals; D001402:B-Lymphocytes; D006183:H-2 Antigens / Q000235:genetics*; D006239:Haplotypes; D009052:Leukemia Virus, Murine; D008223:Lymphoma / Q000235:genetics / Q000276:immunology*; D008285:Major Histocompatibility Complex; D051379:Mice; D008810:Mice, Inbred C57BL; D013601:T-Lymphocytes; D014412:Tumor Virus Infections / Q000235:genetics / Q000276:immunology*
D006183:H-2 Antigens