Regulation of Qa-1 expression and determinant modification by an H-2D-linked gene, Qdm

We examined the regulation of cell surface expression of the Qa-1 alloantigens using a panel of monoclonal anti-Qa-1 cytotoxic T-lymphocyte (mCTL) lines. In contrast to previous reports of tissue-specific expression, we found that Qa-1 was widely expressed, resembling the prototypical class I H-2K/D...

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Bibliographic Details
Published in:Immunogenetics (New York) 1988-11, Vol.28 (5), p.334-344
Main Authors: ALDRICH, C. J, RODGERS, J. R, RICH, R. R
Format: Article
Language:English
Subjects:
Animals
Antigenic determinants, haptens, artificial antigens
Antigens
Biological and medical sciences
Cell Line
Cytotoxicity Tests, Immunologic
Epitopes
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Gene Expression Regulation
Genes, MHC Class I
Genes, Regulator
Genetic Complementation Test
Genetic Linkage
H-2 Antigens - genetics
Histocompatibility Antigens Class I - genetics
Mice - genetics
Mice, Inbred Strains
Molecular immunology
Peptides - genetics
Tissue Distribution
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Summary:We examined the regulation of cell surface expression of the Qa-1 alloantigens using a panel of monoclonal anti-Qa-1 cytotoxic T-lymphocyte (mCTL) lines. In contrast to previous reports of tissue-specific expression, we found that Qa-1 was widely expressed, resembling the prototypical class I H-2K/D molecules. We further found that an H-2D-linked gene, which we termed Qdm for Qa-1 determinant modifier, controlled expression of certain CTL-defined Qa-1 antigenic determinants. H-2Dk homozygous haplotypes expressed a recessive allele of the modifier, Qdmk, whereas all other H-2 haplotypes tested expressed a dominant allele, Qdm+. The Qdm+ allele regulated in trans Qa-1 epitope expression from a Qdmk chromosome, modifying expression of particular CTL-defined Qa-1 antigenic determinants rather than affecting levels of cell surface expression. Mechanisms of Qdm function may include either a novel protein modification system or an unprecedented case of antigen recognition restricted by a nonclassical major histocompatibility complex molecule.
ISSN:0093-7711
1432-1211
DOI:10.1007/BF00364232