Abstract
In humans, interferon gamma (IFN-gamma) receptor deficiency leads to a predisposition to mycobacterial infections and impairs the formation of mature granulomas. Interleukin-12 (IL-12) receptor deficiency was found in otherwise healthy individuals with mycobacterial infections. Mature granulomas were seen, surrounded by T cells and centered with epithelioid and multinucleated giant cells, yet reduced IFN-gamma concentrations were found to be secreted by activated natural killer and T cells. Thus, IL-12-dependent IFN-gamma secretion in humans seems essential in the control of mycobacterial infections, despite the formation of mature granulomas due to IL-12-independent IFN-gamma secretion.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cytotoxicity, Immunologic
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Female
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Granuloma / immunology
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Humans
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Hypersensitivity, Delayed
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Interferon gamma Receptor
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Interferon-gamma / biosynthesis
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Interferon-gamma / immunology
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Interferon-gamma / metabolism
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Interleukin-12 / immunology*
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Killer Cells, Natural / immunology
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Lymphocyte Activation
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Male
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Mice
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Mice, Knockout
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Mutation
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Mycobacterium avium-intracellulare Infection / immunology*
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Mycobacterium bovis*
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Pedigree
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Receptors, Interferon / genetics
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Receptors, Interferon / immunology
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Receptors, Interleukin / deficiency
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Receptors, Interleukin / genetics*
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Receptors, Interleukin-12
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T-Lymphocytes / immunology
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Tuberculosis / immunology*
Substances
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Receptors, Interferon
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Receptors, Interleukin
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Receptors, Interleukin-12
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Interleukin-12
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Interferon-gamma