Abstract
Tapasin is a component of the major histocompatibility complex (MHC) class I antigen-loading complex. Here we show that mice with a disrupted tapasin gene display reduced MHC class I expression. Cytotoxic T cell (CTL) responses to viruses are impaired, and dendritic cells of tapasin-deficient mice do not cross-present protein antigen via the MHC class I pathway, indicating a defect in antigen processing. Natural killer (NK) cells from tapasin-deficient mice have an altered repertoire and are self-tolerant. In addition, the repertoire of class I-bound peptides is altered towards less stably binding ones. Thus tapasin plays a role in CTL and NK immune responses and in optimal peptide selection.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigen Presentation / immunology
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Antiporters / genetics
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Antiporters / immunology*
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Dendritic Cells / immunology
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H-2 Antigens / immunology
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H-2 Antigens / metabolism
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Histocompatibility Antigen H-2D
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Histocompatibility Antigens Class I / genetics
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Histocompatibility Antigens Class I / immunology
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Immune Tolerance / immunology
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Immunoglobulins / deficiency
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Immunoglobulins / genetics
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Immunoglobulins / immunology*
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Killer Cells, Natural / cytology
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Killer Cells, Natural / immunology*
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Membrane Transport Proteins
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Mice
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Mice, Knockout
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Peptides / immunology*
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Peptides / metabolism
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Phenotype
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T-Lymphocytes, Cytotoxic / immunology*
Substances
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Antiporters
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H-2 Antigens
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H-2Kb protein, mouse
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Histocompatibility Antigen H-2D
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Histocompatibility Antigens Class I
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Immunoglobulins
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Membrane Transport Proteins
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Peptides
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tapasin