Abstract
Natural killer (NK) cells are believed to achieve self-tolerance through the expression of self-MHC-specific inhibitory receptors, such as members of the Ly49 and CD94/NKG2 families. Individual Ly49 genes are stochastically expressed by NK subsets and are expressed in a monoallelic fashion, but little is known about the mechanisms underlying CD94/NKG2A expression. We show here that, like Ly49 genes, mouse Nkg2a is stochastically and monoallelically expressed. Thus, a single general mechanism controls expression of all known MHC-specific receptors by mouse NK cells. In addition, we find that DBA/2J mice are naturally CD94-deficient and do not express cell-surface CD94/NKG2A receptors, even on neonatal NK cells. Thus, self-tolerance of neonatal NK cells cannot be attributed to CD94/NKG2A expression. Taken together, the results lead to a reconsideration of current models of NK cell development and self-tolerance.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Alleles
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Animals
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Animals, Newborn
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Antibodies, Monoclonal
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Antibody Specificity
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Antigens, CD / genetics
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Antigens, Ly*
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Cell Differentiation
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Gene Expression
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Killer Cells, Natural / cytology
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Killer Cells, Natural / immunology*
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Lectins, C-Type*
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Membrane Glycoproteins / deficiency*
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Membrane Glycoproteins / genetics
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Mice
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Mice, Inbred BALB C
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Mice, Inbred DBA
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Mice, Transgenic
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Models, Immunological
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NK Cell Lectin-Like Receptor Subfamily C
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NK Cell Lectin-Like Receptor Subfamily D
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Receptors, Immunologic / genetics*
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Receptors, NK Cell Lectin-Like
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Receptors, Natural Killer Cell
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Self Tolerance
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T-Lymphocyte Subsets / immunology
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Thymus Gland / immunology
Substances
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Antibodies, Monoclonal
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Antigens, CD
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Antigens, Ly
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Klrc1 protein, mouse
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Klrd1 protein, mouse
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Lectins, C-Type
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Membrane Glycoproteins
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NK Cell Lectin-Like Receptor Subfamily C
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NK Cell Lectin-Like Receptor Subfamily D
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Receptors, Immunologic
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Receptors, NK Cell Lectin-Like
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Receptors, Natural Killer Cell