TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine
T H 17 cells are major drivers of inflammation and involved in several autoimmune diseases. Tissue inflammation is a beneficial host response to infection, but it can also contribute to autoimmunity. The crosstalk between a tissue and the immune system during an inflammatory response is key for pres...
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Veröffentlicht in: | Mucosal immunology 2017-11, Vol.10 (6), p.1431-1442 |
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creator | Pascual-Reguant, A Bayat Sarmadi, J Baumann, C Noster, R Cirera-Salinas, D Curato, C Pelczar, P Huber, S Zielinski, C E Löhning, M Hauser, A E Esplugues, E |
description | T
H
17 cells are major drivers of inflammation and involved in several autoimmune diseases. Tissue inflammation is a beneficial host response to infection, but it can also contribute to autoimmunity. The crosstalk between a tissue and the immune system during an inflammatory response is key for preserving tissue integrity and restoring physiological processes. However, how the inflamed tissue regulates the magnitude of an immune response by controlling pro-inflammatory T cells is not well characterized so far. Here we show that T
H
17 cells accumulating in the small intestine upon inflammation express the IL-33 receptor (ST2) and intestinal epithelial cells (IEC) are the main source of the alarmin interleukin-33 (IL-33). We show that pro-inflammatory T
H
17 cells acquire a regulatory phenotype with immunosuppressive properties in response to IL-33. Absence of ST2 signaling promotes the secretion of pro-inflammatory cytokines by T
H
17 cells and dampens the secretion of IL-10. Our results provide new insights into the mechanisms by which IEC, via IL-33/ST2 axis, may control pro-inflammatory T
H
17 cells in the small intestine to sustain homeostasis. |
doi_str_mv | 10.1038/mi.2017.5 |
format | Article |
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H
17 cells are major drivers of inflammation and involved in several autoimmune diseases. Tissue inflammation is a beneficial host response to infection, but it can also contribute to autoimmunity. The crosstalk between a tissue and the immune system during an inflammatory response is key for preserving tissue integrity and restoring physiological processes. However, how the inflamed tissue regulates the magnitude of an immune response by controlling pro-inflammatory T cells is not well characterized so far. Here we show that T
H
17 cells accumulating in the small intestine upon inflammation express the IL-33 receptor (ST2) and intestinal epithelial cells (IEC) are the main source of the alarmin interleukin-33 (IL-33). We show that pro-inflammatory T
H
17 cells acquire a regulatory phenotype with immunosuppressive properties in response to IL-33. Absence of ST2 signaling promotes the secretion of pro-inflammatory cytokines by T
H
17 cells and dampens the secretion of IL-10. Our results provide new insights into the mechanisms by which IEC, via IL-33/ST2 axis, may control pro-inflammatory T
H
17 cells in the small intestine to sustain homeostasis.</description><identifier>ISSN: 1933-0219</identifier><identifier>EISSN: 1935-3456</identifier><identifier>DOI: 10.1038/mi.2017.5</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>631/250/127/1213 ; 631/250/1619/554/1898/1273 ; 631/250/249/1313 ; 631/250/347 ; Allergology ; Antibodies ; Autoimmune diseases ; Biomedical and Life Sciences ; Biomedicine ; Epithelial cells ; Gastroenterology ; Helper cells ; Homeostasis ; Immunology ; Inflammation ; Interleukin 10 ; Lymphocytes T ; Phenotypes ; Small intestine</subject><ispartof>Mucosal immunology, 2017-11, Vol.10 (6), p.1431-1442</ispartof><rights>Society for Mucosal Immunology 2017</rights><rights>Copyright Nature Publishing Group Nov 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-1961f2486c0417228cad53ced5a5fc3bcc2ac666d783631bf080882a7c21cce63</citedby><cites>FETCH-LOGICAL-c356t-1961f2486c0417228cad53ced5a5fc3bcc2ac666d783631bf080882a7c21cce63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1951516616?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,64384,64386,64388,72240</link.rule.ids></links><search><creatorcontrib>Pascual-Reguant, A</creatorcontrib><creatorcontrib>Bayat Sarmadi, J</creatorcontrib><creatorcontrib>Baumann, C</creatorcontrib><creatorcontrib>Noster, R</creatorcontrib><creatorcontrib>Cirera-Salinas, D</creatorcontrib><creatorcontrib>Curato, C</creatorcontrib><creatorcontrib>Pelczar, P</creatorcontrib><creatorcontrib>Huber, S</creatorcontrib><creatorcontrib>Zielinski, C E</creatorcontrib><creatorcontrib>Löhning, M</creatorcontrib><creatorcontrib>Hauser, A E</creatorcontrib><creatorcontrib>Esplugues, E</creatorcontrib><title>TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine</title><title>Mucosal immunology</title><addtitle>Mucosal Immunol</addtitle><description>T
H
17 cells are major drivers of inflammation and involved in several autoimmune diseases. Tissue inflammation is a beneficial host response to infection, but it can also contribute to autoimmunity. The crosstalk between a tissue and the immune system during an inflammatory response is key for preserving tissue integrity and restoring physiological processes. However, how the inflamed tissue regulates the magnitude of an immune response by controlling pro-inflammatory T cells is not well characterized so far. Here we show that T
H
17 cells accumulating in the small intestine upon inflammation express the IL-33 receptor (ST2) and intestinal epithelial cells (IEC) are the main source of the alarmin interleukin-33 (IL-33). We show that pro-inflammatory T
H
17 cells acquire a regulatory phenotype with immunosuppressive properties in response to IL-33. Absence of ST2 signaling promotes the secretion of pro-inflammatory cytokines by T
H
17 cells and dampens the secretion of IL-10. Our results provide new insights into the mechanisms by which IEC, via IL-33/ST2 axis, may control pro-inflammatory T
H
17 cells in the small intestine to sustain homeostasis.</description><subject>631/250/127/1213</subject><subject>631/250/1619/554/1898/1273</subject><subject>631/250/249/1313</subject><subject>631/250/347</subject><subject>Allergology</subject><subject>Antibodies</subject><subject>Autoimmune diseases</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Epithelial cells</subject><subject>Gastroenterology</subject><subject>Helper cells</subject><subject>Homeostasis</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Interleukin 10</subject><subject>Lymphocytes T</subject><subject>Phenotypes</subject><subject>Small intestine</subject><issn>1933-0219</issn><issn>1935-3456</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkE9LAzEQxYMoWKsHv0HAiwpbM5kmmz1K8U-h4MH2HNJsVrdkd2uyBfvtzVoPoqd5M_x4M_MIuQQ2AYbqrqknnEE-EUdkBAWKDKdCHn9rzBiH4pScxbhhTDImcERWy2fIqXXeR-o-t8HFSF-XnJq2pCY4aru2D533rqTrPe3fHTXehKZu6XyRIdIkhmFsjPep6V3s69adk5PK-OgufuqYrB4flrPnbPHyNJ_dLzKLQvYZFBIqPlXSsinknCtrSoHWlcKIyuLaWm6slLLMFUqEdcUUU4qb3HKw1kkck-uD7zZ0H7u0Wzd1HJ4xret2UYOSKmeIMk_o1R900-1Cm67TUAgQICUMhjcHyoYuxuAqvQ11Y8JeA9NDwGmBHgLWIrG3BzYmpn1z4ZfjP_gLWDx49g</recordid><startdate>20171101</startdate><enddate>20171101</enddate><creator>Pascual-Reguant, A</creator><creator>Bayat Sarmadi, J</creator><creator>Baumann, C</creator><creator>Noster, R</creator><creator>Cirera-Salinas, D</creator><creator>Curato, C</creator><creator>Pelczar, P</creator><creator>Huber, S</creator><creator>Zielinski, C E</creator><creator>Löhning, M</creator><creator>Hauser, A E</creator><creator>Esplugues, E</creator><general>Nature Publishing Group US</general><general>Elsevier Limited</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</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>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20171101</creationdate><title>TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine</title><author>Pascual-Reguant, A ; Bayat Sarmadi, J ; Baumann, C ; Noster, R ; Cirera-Salinas, D ; Curato, C ; Pelczar, P ; Huber, S ; Zielinski, C E ; Löhning, M ; Hauser, A E ; Esplugues, E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-1961f2486c0417228cad53ced5a5fc3bcc2ac666d783631bf080882a7c21cce63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>631/250/127/1213</topic><topic>631/250/1619/554/1898/1273</topic><topic>631/250/249/1313</topic><topic>631/250/347</topic><topic>Allergology</topic><topic>Antibodies</topic><topic>Autoimmune diseases</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Epithelial cells</topic><topic>Gastroenterology</topic><topic>Helper cells</topic><topic>Homeostasis</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Interleukin 10</topic><topic>Lymphocytes T</topic><topic>Phenotypes</topic><topic>Small intestine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pascual-Reguant, A</creatorcontrib><creatorcontrib>Bayat Sarmadi, J</creatorcontrib><creatorcontrib>Baumann, C</creatorcontrib><creatorcontrib>Noster, R</creatorcontrib><creatorcontrib>Cirera-Salinas, D</creatorcontrib><creatorcontrib>Curato, C</creatorcontrib><creatorcontrib>Pelczar, P</creatorcontrib><creatorcontrib>Huber, S</creatorcontrib><creatorcontrib>Zielinski, C E</creatorcontrib><creatorcontrib>Löhning, M</creatorcontrib><creatorcontrib>Hauser, A E</creatorcontrib><creatorcontrib>Esplugues, E</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Mucosal immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pascual-Reguant, A</au><au>Bayat Sarmadi, J</au><au>Baumann, C</au><au>Noster, R</au><au>Cirera-Salinas, D</au><au>Curato, C</au><au>Pelczar, P</au><au>Huber, S</au><au>Zielinski, C E</au><au>Löhning, M</au><au>Hauser, A E</au><au>Esplugues, E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine</atitle><jtitle>Mucosal immunology</jtitle><stitle>Mucosal Immunol</stitle><date>2017-11-01</date><risdate>2017</risdate><volume>10</volume><issue>6</issue><spage>1431</spage><epage>1442</epage><pages>1431-1442</pages><issn>1933-0219</issn><eissn>1935-3456</eissn><abstract>T
H
17 cells are major drivers of inflammation and involved in several autoimmune diseases. Tissue inflammation is a beneficial host response to infection, but it can also contribute to autoimmunity. The crosstalk between a tissue and the immune system during an inflammatory response is key for preserving tissue integrity and restoring physiological processes. However, how the inflamed tissue regulates the magnitude of an immune response by controlling pro-inflammatory T cells is not well characterized so far. Here we show that T
H
17 cells accumulating in the small intestine upon inflammation express the IL-33 receptor (ST2) and intestinal epithelial cells (IEC) are the main source of the alarmin interleukin-33 (IL-33). We show that pro-inflammatory T
H
17 cells acquire a regulatory phenotype with immunosuppressive properties in response to IL-33. Absence of ST2 signaling promotes the secretion of pro-inflammatory cytokines by T
H
17 cells and dampens the secretion of IL-10. Our results provide new insights into the mechanisms by which IEC, via IL-33/ST2 axis, may control pro-inflammatory T
H
17 cells in the small intestine to sustain homeostasis.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><doi>10.1038/mi.2017.5</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 631/250/127/1213 631/250/1619/554/1898/1273 631/250/249/1313 631/250/347 Allergology Antibodies Autoimmune diseases Biomedical and Life Sciences Biomedicine Epithelial cells Gastroenterology Helper cells Homeostasis Immunology Inflammation Interleukin 10 Lymphocytes T Phenotypes Small intestine |
title | TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine |
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