Phosphatase SHP-1 promotes TLR- and RIG-I-activated production of type I interferon by inhibiting the kinase IRAK1
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 phospha...
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| Veröffentlicht in: | Nature immunology 2008-05, Vol.9 (5), p.542-550 |
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| creator | An, Huazhang Hou, Jin Zhou, Jun Zhao, Wei Xu, Hongmei Zheng, Yuejuan Yu, Yizhi Liu, Shuxun Cao, Xuetao |
| description | 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-κB 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. |
| doi_str_mv | 10.1038/ni.1604 |
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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-κB 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.</description><identifier>ISSN: 1529-2908</identifier><identifier>EISSN: 1529-2916</identifier><identifier>DOI: 10.1038/ni.1604</identifier><identifier>PMID: 18391954</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Catalytic Domain - physiology ; Cell receptors ; Cytokines - biosynthesis ; Health aspects ; Homeostasis - immunology ; Immune response ; Immunity, Innate ; Immunology ; Infectious Diseases ; Interferon ; Interferon Regulatory Factor-1 - metabolism ; Interferon Type I - biosynthesis ; Interleukin-1 Receptor-Associated Kinases - antagonists & inhibitors ; Interleukin-1 Receptor-Associated Kinases - chemistry ; Interleukin-1 Receptor-Associated Kinases - metabolism ; Macrophages, Peritoneal ; Membrane Proteins - immunology ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors ; Mitogen-Activated Protein Kinase Kinases - metabolism ; Nerve Tissue Proteins - immunology ; Nerve Tissue Proteins - metabolism ; NF-kappa B - antagonists & inhibitors ; NF-kappa B - metabolism ; Physiological aspects ; Protein Binding ; Protein kinases ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 - immunology ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism ; Signal Transduction ; Toll-Like Receptors - immunology ; Toll-Like Receptors - metabolism</subject><ispartof>Nature immunology, 2008-05, Vol.9 (5), p.542-550</ispartof><rights>Springer Nature America, Inc. 2008</rights><rights>COPYRIGHT 2008 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group May 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c569t-d99b81bef9780bff18dfcbcaca12c579d6828de1306a0123405a401d44f09a6f3</citedby><cites>FETCH-LOGICAL-c569t-d99b81bef9780bff18dfcbcaca12c579d6828de1306a0123405a401d44f09a6f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ni.1604$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ni.1604$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18391954$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>An, Huazhang</creatorcontrib><creatorcontrib>Hou, Jin</creatorcontrib><creatorcontrib>Zhou, Jun</creatorcontrib><creatorcontrib>Zhao, Wei</creatorcontrib><creatorcontrib>Xu, Hongmei</creatorcontrib><creatorcontrib>Zheng, Yuejuan</creatorcontrib><creatorcontrib>Yu, Yizhi</creatorcontrib><creatorcontrib>Liu, Shuxun</creatorcontrib><creatorcontrib>Cao, Xuetao</creatorcontrib><title>Phosphatase SHP-1 promotes TLR- and RIG-I-activated production of type I interferon by inhibiting the kinase IRAK1</title><title>Nature immunology</title><addtitle>Nat Immunol</addtitle><addtitle>Nat Immunol</addtitle><description>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-κB 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.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Catalytic Domain - physiology</subject><subject>Cell receptors</subject><subject>Cytokines - biosynthesis</subject><subject>Health aspects</subject><subject>Homeostasis - immunology</subject><subject>Immune response</subject><subject>Immunity, Innate</subject><subject>Immunology</subject><subject>Infectious Diseases</subject><subject>Interferon</subject><subject>Interferon Regulatory Factor-1 - metabolism</subject><subject>Interferon Type I - biosynthesis</subject><subject>Interleukin-1 Receptor-Associated Kinases - antagonists & inhibitors</subject><subject>Interleukin-1 Receptor-Associated Kinases - chemistry</subject><subject>Interleukin-1 Receptor-Associated Kinases - metabolism</subject><subject>Macrophages, Peritoneal</subject><subject>Membrane Proteins - immunology</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors</subject><subject>Mitogen-Activated Protein Kinase Kinases - metabolism</subject><subject>Nerve Tissue Proteins - immunology</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>NF-kappa B - antagonists & inhibitors</subject><subject>NF-kappa B - metabolism</subject><subject>Physiological aspects</subject><subject>Protein Binding</subject><subject>Protein kinases</subject><subject>Protein Tyrosine Phosphatase, Non-Receptor Type 6 - immunology</subject><subject>Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism</subject><subject>Signal Transduction</subject><subject>Toll-Like Receptors - immunology</subject><subject>Toll-Like Receptors - metabolism</subject><issn>1529-2908</issn><issn>1529-2916</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqF0luP1CAUAODGaNyLxn9giCZeHjoCpRQeJxvdbZzEzez6TCiFGdYpjEDNzr-XZiZuZmM0faDAx4FzcoriFYIzBCv2ydkZopA8KU5RjXmJOaJP__xDdlKcxXgHISINJc-LE8QqjnhNTotwvfZxu5ZJRg1urq5LBLbBDz7pCG4XyxJI14Nle1m2pVTJ_pJJ95PoxzzzDngD0m6rQQusSzoYHfJit8uzte1ssm4F0lqDH9ZNF7TL-Vf0onhm5Cbql4fxvPj-5fPtxVW5-HbZXswXpaopT2XPecdQpw1vGOyMQaw3qlNSSYRV3fCeMsx6jSpIJUS4IrCWBKKeEAO5pKY6L97v4-bn_hx1TGKwUenNRjrtxyhYXRGaC4WzfPdPmRXGuc7_hRhSyirMMnzzCN75MbicrsAYN_mtnGf0do9WcqOFdcanINUUUcwRhxQ1iJGsZn9R-ev1YJV32ti8fnTg49GBbJK-Tys5xijam-WxPdRIBR9j0EZsgx1k2AkExdRZwlkxdVaWrw8Zjd2g-wd3aKUMPuxBzFtupcNDyo9j_QYiP9FO</recordid><startdate>20080501</startdate><enddate>20080501</enddate><creator>An, Huazhang</creator><creator>Hou, Jin</creator><creator>Zhou, Jun</creator><creator>Zhao, Wei</creator><creator>Xu, Hongmei</creator><creator>Zheng, Yuejuan</creator><creator>Yu, Yizhi</creator><creator>Liu, Shuxun</creator><creator>Cao, Xuetao</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISR</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20080501</creationdate><title>Phosphatase SHP-1 promotes TLR- and RIG-I-activated production of type I interferon by inhibiting the kinase IRAK1</title><author>An, Huazhang ; Hou, Jin ; Zhou, Jun ; Zhao, Wei ; Xu, Hongmei ; Zheng, Yuejuan ; Yu, Yizhi ; Liu, Shuxun ; Cao, Xuetao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c569t-d99b81bef9780bff18dfcbcaca12c579d6828de1306a0123405a401d44f09a6f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Catalytic Domain - 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Academic</collection><jtitle>Nature immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>An, Huazhang</au><au>Hou, Jin</au><au>Zhou, Jun</au><au>Zhao, Wei</au><au>Xu, Hongmei</au><au>Zheng, Yuejuan</au><au>Yu, Yizhi</au><au>Liu, Shuxun</au><au>Cao, Xuetao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Phosphatase SHP-1 promotes TLR- and RIG-I-activated production of type I interferon by inhibiting the kinase IRAK1</atitle><jtitle>Nature immunology</jtitle><stitle>Nat Immunol</stitle><addtitle>Nat Immunol</addtitle><date>2008-05-01</date><risdate>2008</risdate><volume>9</volume><issue>5</issue><spage>542</spage><epage>550</epage><pages>542-550</pages><issn>1529-2908</issn><eissn>1529-2916</eissn><abstract>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-κB 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.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>18391954</pmid><doi>10.1038/ni.1604</doi><tpages>9</tpages></addata></record> |
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| subjects | Animals Biomedical and Life Sciences Biomedicine Catalytic Domain - physiology Cell receptors Cytokines - biosynthesis Health aspects Homeostasis - immunology Immune response Immunity, Innate Immunology Infectious Diseases Interferon Interferon Regulatory Factor-1 - metabolism Interferon Type I - biosynthesis Interleukin-1 Receptor-Associated Kinases - antagonists & inhibitors Interleukin-1 Receptor-Associated Kinases - chemistry Interleukin-1 Receptor-Associated Kinases - metabolism Macrophages, Peritoneal Membrane Proteins - immunology Membrane Proteins - metabolism Mice Mice, Inbred C57BL Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinase Kinases - metabolism Nerve Tissue Proteins - immunology Nerve Tissue Proteins - metabolism NF-kappa B - antagonists & inhibitors NF-kappa B - metabolism Physiological aspects Protein Binding Protein kinases Protein Tyrosine Phosphatase, Non-Receptor Type 6 - immunology Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism Signal Transduction Toll-Like Receptors - immunology Toll-Like Receptors - metabolism |
| title | Phosphatase SHP-1 promotes TLR- and RIG-I-activated production of type I interferon by inhibiting the kinase IRAK1 |
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