| Toll-like receptor-mediated inhibition of Gas6 and ProS expression facilitates inflammatory cytokine production in mouse macrophages. | |
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MedLine Citation:
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PMID: 22043818 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Activation of Toll-like receptors (TLRs) triggers rapid inflammatory cytokine production in various cell types. The exogenous product of growth-arrest-specific gene 6 (Gas6) and Protein S (ProS) inhibit the TLR-triggered inflammatory responses through the activation of Tyro3, Axl and Mer (TAM) receptors. However, regulation of the Gas6/ProS-TAM system remains largely unknown. In the current study, mouse macrophages are shown to constitutively express Gas6 and ProS, which synergistically suppress the basal and TLR-triggered production of inflammatory cytokines, including those of tumor necrosis factor alpha and interleukins (IL)-6 and IL-1β, by the macrophages in an autocrine manner. Notably, TLR signaling markedly decreases Gas6 and ProS expression in macrophages through the activation of the nuclear factor-κB. Further, the down-regulation of Gas6 and ProS by TLR signaling facilitates the TLR-mediated inflammatory cytokine production in mouse macrophages. These results describe a self-regulatory mechanism of TLR signaling through the suppression of Gas6 and ProS expression. |
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Authors:
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Tingting Deng; Yue Zhang; Qiaoyuan Chen; Keqin Yan; Daishu Han |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-9-27 |
Journal Detail:
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Title: Immunology Volume: - ISSN: 1365-2567 ISO Abbreviation: - Publication Date: 2011 Sep |
Date Detail:
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Created Date: 2011-11-2 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0374672 Medline TA: Immunology Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Journal compilation © 2011 Blackwell Publishing Ltd. |
Affiliation:
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Department of Cell Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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