Abstract
Mechanisms that control the activation of antigen-specific immune responses in vivo are poorly understood. It has been suggested that the initiation of adaptive immune responses is controlled by innate immune recognition. Mammalian Toll-like receptors play an essential role in innate immunity by recognizing conserved pathogen-associated molecular patterns and initiating the activation of NF-kappaB and other signaling pathways through the adapter protein, MyD88. Here we show that MyD88-deficient mice have a profound defect in the activation of antigen-specific T helper type 1 (TH1) but not TH2 immune responses. These results suggest that distinct pathways of the innate immune system control activation of the two effector arms of adaptive immunity.
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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Adaptor Proteins, Signal Transducing
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Animals
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Antigens, Differentiation / genetics*
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Caspase 1 / genetics
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Cell Differentiation
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Cells, Cultured
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Dendritic Cells / immunology
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Drosophila Proteins*
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Immunoglobulins / biosynthesis
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Interferon-gamma / biosynthesis
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Interleukin-13 / biosynthesis
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Lymphocyte Activation*
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Membrane Glycoproteins / physiology*
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Mice
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Mice, Knockout
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Myeloid Differentiation Factor 88
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Phenotype
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Receptors, Cell Surface / physiology*
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Receptors, Immunologic*
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Th1 Cells / immunology*
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Th2 Cells / immunology
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Toll-Like Receptors
Substances
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Adaptor Proteins, Signal Transducing
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Antigens, Differentiation
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Drosophila Proteins
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Immunoglobulins
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Interleukin-13
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Membrane Glycoproteins
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Myd88 protein, mouse
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Myeloid Differentiation Factor 88
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Receptors, Cell Surface
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Receptors, Immunologic
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Toll-Like Receptors
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Interferon-gamma
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Caspase 1