Abstract
Naive T cells respond to antigens by differentiating into effector and regulatory lineages. Whereas the roles of T cell-intrinsic pathways have been extensively studied, how T cell lineage choices are controlled by innate immune signals remains elusive. Here we report that dendritic cell (DC)-expressed phosphatase MKP-1, a negative regulator of the MAP kinases, programmed reciprocal T helper 1 (Th1) and Th17 cell differentiation by modulating IL-12-STAT4 and IL-6-STAT3 axes and cytokine receptor expression at the DC-T cell interface. MKP-1 was regulated by innate recognition signals and its deficiency disrupted antimicrobial responses and promoted T cell-mediated inflammation. Moreover, MKP-1 inhibited induction of regulatory T cells by downregulating TGF-β2 production from DCs. Our findings identify a regulatory circuit linking MKP-1 signaling in DCs, production of polarizing cytokines, and integration of DC-derived signals in responding T cells, that bridges innate and adaptive immunity to coordinate protective immunity and immunopathology.
Copyright © 2011 Elsevier Inc. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptive Immunity
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Adoptive Transfer
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Animals
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Candidiasis / immunology*
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Cell Communication
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Cell Differentiation
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Cells, Cultured
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Cytokines / genetics
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Cytokines / metabolism
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Dendritic Cells / immunology
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Dendritic Cells / metabolism*
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Dendritic Cells / pathology
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Dual Specificity Phosphatase 1 / genetics
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Dual Specificity Phosphatase 1 / immunology
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Dual Specificity Phosphatase 1 / metabolism*
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Dual Specificity Phosphatase 1 / pharmacology
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Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors
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Immunity, Innate
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Listeriosis / immunology*
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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STAT3 Transcription Factor / metabolism
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STAT4 Transcription Factor / metabolism
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Signal Transduction / immunology
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T-Lymphocytes, Regulatory / immunology
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T-Lymphocytes, Regulatory / metabolism*
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T-Lymphocytes, Regulatory / pathology
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Th1 Cells / immunology
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Th1 Cells / metabolism
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Th1 Cells / pathology
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Th1-Th2 Balance
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Th17 Cells / immunology
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Th17 Cells / metabolism
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Th17 Cells / pathology
Substances
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Cytokines
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STAT3 Transcription Factor
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STAT4 Transcription Factor
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Extracellular Signal-Regulated MAP Kinases
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Dual Specificity Phosphatase 1