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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2008-4-21
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pubmed:abstractText |
Unbalanced production of proinflammatory cytokines and type I interferons in immune responses may lead to immunopathology; thus, the mechanisms that ensure the beneficial production of proinflammatory cytokines and type I interferons are of particular importance. Here we demonstrate that the phosphatase SHP-1 negatively regulated Toll-like receptor-mediated production of proinflammatory cytokines by inhibiting activation of the transcription factor NF-kappaB and mitogen-activated protein kinase. Simultaneously, SHP-1 increased the production of type I interferon mediated by Toll-like receptors and the helicase RIG-I by directly binding to and inhibiting activation of the kinase IRAK1. Our data demonstrate that SHP-1 contributes to immune homeostasis by balancing the production of proinflammatory cytokines and type I interferons in the innate immune response.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factor-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1 Receptor-Associated...,
http://linkedlifedata.com/resource/pubmed/chemical/Irak1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase...,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Tyrosine Phosphatase...,
http://linkedlifedata.com/resource/pubmed/chemical/Robo3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1529-2916
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
9
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
542-50
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pubmed:dateRevised |
2011-3-18
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pubmed:meshHeading |
pubmed-meshheading:18391954-Animals,
pubmed-meshheading:18391954-Catalytic Domain,
pubmed-meshheading:18391954-Cytokines,
pubmed-meshheading:18391954-Homeostasis,
pubmed-meshheading:18391954-Immunity, Innate,
pubmed-meshheading:18391954-Interferon Regulatory Factor-1,
pubmed-meshheading:18391954-Interferon Type I,
pubmed-meshheading:18391954-Interleukin-1 Receptor-Associated Kinases,
pubmed-meshheading:18391954-Macrophages, Peritoneal,
pubmed-meshheading:18391954-Membrane Proteins,
pubmed-meshheading:18391954-Mice,
pubmed-meshheading:18391954-Mice, Inbred C57BL,
pubmed-meshheading:18391954-Mitogen-Activated Protein Kinase Kinases,
pubmed-meshheading:18391954-NF-kappa B,
pubmed-meshheading:18391954-Nerve Tissue Proteins,
pubmed-meshheading:18391954-Protein Binding,
pubmed-meshheading:18391954-Protein Tyrosine Phosphatase, Non-Receptor Type 6,
pubmed-meshheading:18391954-Signal Transduction,
pubmed-meshheading:18391954-Toll-Like Receptors
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pubmed:year |
2008
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pubmed:articleTitle |
Phosphatase SHP-1 promotes TLR- and RIG-I-activated production of type I interferon by inhibiting the kinase IRAK1.
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pubmed:affiliation |
Institute of Immunology and National Key Laboratory of Medical Immunology, Second Military Medical University, Shanghai 200433, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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