Abstract
Toll-like receptors (TLRs) control activation of adaptive immune responses by antigen-presenting cells (APCs). However, initiation of adaptive immune responses is also controlled by regulatory T cells (TR cells), which act to prevent activation of autoreactive T cells. Here we describe a second mechanism of immune induction by TLRs, which is independent of effects on costimulation. Microbial induction of the Toll pathway blocked the suppressive effect of CD4+CD25+ TR cells, allowing activation of pathogen-specific adaptive immune responses. This block of suppressor activity was dependent in part on interleukin-6, which was induced by TLRs upon recognition of microbial products.
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, CD / immunology
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Antigens, CD / metabolism
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Antigens, Differentiation / metabolism
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Cells, Cultured
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Culture Media, Conditioned
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Dendritic Cells / immunology*
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Dendritic Cells / metabolism
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Dinucleoside Phosphates / immunology
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Drosophila Proteins*
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Immune Tolerance*
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Immunization
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Interleukin-6 / metabolism
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Interleukin-6 / physiology*
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Lipopolysaccharides / immunology
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Lymphocyte Activation
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Membrane Glycoproteins / physiology*
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Mice
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Mice, Inbred C57BL
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Myeloid Differentiation Factor 88
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Ovalbumin / immunology
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Receptors, Cell Surface / physiology*
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Receptors, Immunologic / metabolism
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Self Tolerance
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T-Lymphocytes / immunology
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T-Lymphocytes, Regulatory / immunology*
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Toll-Like Receptors
Substances
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Adaptor Proteins, Signal Transducing
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Antigens, CD
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Antigens, Differentiation
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Culture Media, Conditioned
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Dinucleoside Phosphates
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Drosophila Proteins
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Interleukin-6
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Lipopolysaccharides
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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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cytidylyl-3'-5'-guanosine
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Ovalbumin