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H‐2D CONTROL OF LEUKAEMIA SUSCEPTIBILITY: MECHANISM AND IMPLICATIONS *
Author(s) -
Meruelo D.
Publication year - 1980
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.1980.tb00710.x
Subject(s) - biology , virus , antigen , virology , gene , major histocompatibility complex , immune system , transcription (linguistics) , gene expression , immunology , genetics , linguistics , philosophy
Summary Genes in the D region of the murine major histocompatibility complex, H‐2, confer resistance to radiation‐induced leukaemia virus. H‐2D gene control appears to ensue at a step subsequent to virus infection, since elimination of virus infected cells does not become apparent until 3‐5 weeks after virus infection. Nonetheless, almost immediately after virus infection, expression of H‐2D‐coded antigens is markedly elevated on the surface of thymocytes from resistant (H‐2D d ) but not susceptible mice (H‐2D s or H‐2D q ). This increased H‐2D antigen expression triggers a vigorous cell‐mediated immune response which probably plays a key role in resistance to leukaemia via elimination of virus‐infected cells. A hypothesis is put forth to explain the induction of increased sythesis and expression of H‐2D antigens. This hypothesis postulates that the oncogenic segment of RadLV bears a close resemblance to H‐2.4, the private specificity for H‐2D d , allowing it to integrate at or near the H‐2D d murine gene. Subsequent to integration, the rates of transcription and translation are altered with a resulting increase in cell surface antigen expression. Other possibilities are also discussed.