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THE H‐2 COMPLEX REGULATES BOTH THE SUSCEPTIBILITY TO MOUSE VIRAL LYMPHOMAGENESIS AND THE PHENOTYPE OF THE VIRUS‐INDUCED LYMPHOMAS
Author(s) -
Zijlstra M.,
Vasmel W. L. E.,
Radaskiewicz T.,
Matthews E.,
Melief C. J. M.
Publication year - 1986
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/j.1744-313x.1986.tb01086.x
Subject(s) - phenotype , virology , virus , biology , lymphoma , immunology , genetics , gene
SUMMARY Neonatal infection of C57BL/10 mice with cloned ecotropic and/or dual‐tropic 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: (a) Resistance to the early development of T cell lymphomas is controlled by the H‐21‐A locus. (b) 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. (c) B10 ( H‐2 b ) 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‐2 a mice. The possible response mechanisms which underlie these observations, including: (1) I‐A ‐regulated immunoselection against MuLV antigens expressed by (pre) leukaemic T cells, (2) aberrant expression of class II MHC antigens on some B cell lymphomas and (3) I‐A‐regulated chronic immunostimulation of MuLV‐expressing (pre) leukaemic B cells, are discussed.