Abstract
The mechanisms underlying the profound suppression of cell-mediated immunity (CMI) accompanying measles are unclear. Interleukin-12 (IL-12), derived principally from monocytes and macrophages, is critical for the generation of CMI. Measles virus (MV) infection of primary human monocytes specifically down-regulated IL-12 production. Cross-linking of CD46, a complement regulatory protein that is the cellular receptor for MV, with antibody or with the complement activation product C3b similarly inhibited monocyte IL-12 production, providing a plausible mechanism for MV-induced immunosuppression. CD46 provides a regulatory link between the complement system and cellular immune responses.
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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Antibodies, Monoclonal
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Antigens, CD / immunology
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Antigens, CD / physiology*
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Binding Sites
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Cells, Cultured
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Chemokines / biosynthesis
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Complement C3b / immunology
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Complement C3b / physiology
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Cytokines / biosynthesis
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Down-Regulation
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Humans
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Immune Tolerance*
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Interleukin-10 / physiology
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Interleukin-12 / biosynthesis*
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Measles virus / immunology*
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Measles virus / metabolism
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Membrane Cofactor Protein
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Membrane Glycoproteins / immunology
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Membrane Glycoproteins / physiology*
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Monocytes / immunology*
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Monocytes / virology*
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Receptors, Virus / immunology
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Receptors, Virus / physiology*
Substances
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Antibodies, Monoclonal
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Antigens, CD
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CD46 protein, human
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Chemokines
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Cytokines
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Membrane Cofactor Protein
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Membrane Glycoproteins
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Receptors, Virus
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Interleukin-10
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Interleukin-12
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Complement C3b