Regulating the mucosal immune system: the contrasting roles of LIGHT, HVEM, and their various partners
LIGHT and herpes virus entry mediator (HVEM) comprise a ligand–receptor pair in the tumor necrosis factor superfamily. These molecules play an important role in regulating immunity, particularly in the intestinal mucosa. LIGHT also binds the lymphotoxin β receptor, and HVEM can act as a ligand for i...
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Veröffentlicht in: | Seminars in immunopathology 2009-07, Vol.31 (2), p.207-221 |
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description | LIGHT and herpes virus entry mediator (HVEM) comprise a ligand–receptor pair in the tumor necrosis factor superfamily. These molecules play an important role in regulating immunity, particularly in the intestinal mucosa. LIGHT also binds the lymphotoxin β receptor, and HVEM can act as a ligand for immunoglobulin family molecules, including B- and T-lymphocyte attenuator, which suppresses immune responses. Complexity in this pivotal system arises from several factors, including the non-monogamous pairing of ligands and receptors, and reverse signaling or the ability of some ligands to serve as receptors. As a result, recognition events in this fascinating network of interacting molecules can have pro- or anti-inflammatory consequences. Despite complexity, experiments we and others are carrying out are establishing rules for understanding when and in what cell types these molecules contribute to intestinal inflammation. |
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These molecules play an important role in regulating immunity, particularly in the intestinal mucosa. LIGHT also binds the lymphotoxin β receptor, and HVEM can act as a ligand for immunoglobulin family molecules, including B- and T-lymphocyte attenuator, which suppresses immune responses. Complexity in this pivotal system arises from several factors, including the non-monogamous pairing of ligands and receptors, and reverse signaling or the ability of some ligands to serve as receptors. As a result, recognition events in this fascinating network of interacting molecules can have pro- or anti-inflammatory consequences. Despite complexity, experiments we and others are carrying out are establishing rules for understanding when and in what cell types these molecules contribute to intestinal inflammation.</description><identifier>ISSN: 1863-2297</identifier><identifier>EISSN: 1863-2300</identifier><identifier>DOI: 10.1007/s00281-009-0157-4</identifier><identifier>PMID: 19495760</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Animals ; Antigens ; B-Lymphocytes - immunology ; Biomedical and Life Sciences ; Biomedicine ; Cytokines ; Glycoproteins ; Herpes simplex ; Herpes viruses ; Herpesvirus ; Humans ; Immune response ; Immune system ; Immunity, Mucosal ; Immunoglobulins ; Immunology ; Inflammation ; Inflammation - immunology ; Inflammatory bowel disease ; Internal Medicine ; Intestinal Mucosa - immunology ; Intestine ; Ligands ; Light ; LIGHT protein ; Lymphocytes ; Lymphocytes T ; Lymphotoxin ; Mucosal immunity ; Pathogenesis ; Receptors, Tumor Necrosis Factor, Member 14 - immunology ; Review ; Signal transduction ; T-Lymphocytes - immunology ; Tumor necrosis factor ; Tumor Necrosis Factor Ligand Superfamily Member 14 - immunology ; Tumor necrosis factor-TNF</subject><ispartof>Seminars in immunopathology, 2009-07, Vol.31 (2), p.207-221</ispartof><rights>Springer-Verlag 2009</rights><rights>Springer-Verlag 2009 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-57c956f422ad4f9f8c87e9a0d90bf62e8dcec37a7656a914a9dc23be902d65033</citedby><cites>FETCH-LOGICAL-c499t-57c956f422ad4f9f8c87e9a0d90bf62e8dcec37a7656a914a9dc23be902d65033</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00281-009-0157-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00281-009-0157-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19495760$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Steinberg, Marcos W.</creatorcontrib><creatorcontrib>Shui, Jr-Wen</creatorcontrib><creatorcontrib>Ware, Carl F.</creatorcontrib><creatorcontrib>Kronenberg, Mitchell</creatorcontrib><title>Regulating the mucosal immune system: the contrasting roles of LIGHT, HVEM, and their various partners</title><title>Seminars in immunopathology</title><addtitle>Semin Immunopathol</addtitle><addtitle>Semin Immunopathol</addtitle><description>LIGHT and herpes virus entry mediator (HVEM) comprise a ligand–receptor pair in the tumor necrosis factor superfamily. These molecules play an important role in regulating immunity, particularly in the intestinal mucosa. LIGHT also binds the lymphotoxin β receptor, and HVEM can act as a ligand for immunoglobulin family molecules, including B- and T-lymphocyte attenuator, which suppresses immune responses. Complexity in this pivotal system arises from several factors, including the non-monogamous pairing of ligands and receptors, and reverse signaling or the ability of some ligands to serve as receptors. As a result, recognition events in this fascinating network of interacting molecules can have pro- or anti-inflammatory consequences. Despite complexity, experiments we and others are carrying out are establishing rules for understanding when and in what cell types these molecules contribute to intestinal inflammation.</description><subject>Animals</subject><subject>Antigens</subject><subject>B-Lymphocytes - immunology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cytokines</subject><subject>Glycoproteins</subject><subject>Herpes simplex</subject><subject>Herpes viruses</subject><subject>Herpesvirus</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunity, Mucosal</subject><subject>Immunoglobulins</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Inflammation - immunology</subject><subject>Inflammatory bowel disease</subject><subject>Internal Medicine</subject><subject>Intestinal Mucosa - immunology</subject><subject>Intestine</subject><subject>Ligands</subject><subject>Light</subject><subject>LIGHT protein</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Lymphotoxin</subject><subject>Mucosal immunity</subject><subject>Pathogenesis</subject><subject>Receptors, Tumor Necrosis Factor, Member 14 - immunology</subject><subject>Review</subject><subject>Signal transduction</subject><subject>T-Lymphocytes - immunology</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor Ligand Superfamily Member 14 - immunology</subject><subject>Tumor necrosis factor-TNF</subject><issn>1863-2297</issn><issn>1863-2300</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kV9LHDEUxYNU_Fc_gC8l9KG-OHqTTJJJHwpFrCusCMX2NWQzmXVkJtkmM4Lfvhl3q1ZonxI4v5ycew9CRwROCYA8SwC0IgWAKoBwWZRbaI9UghWUAbz7c6dK7qL9lO4BuGRc7qBdokrFpYA91Hx3y7EzQ-uXeLhzuB9tSKbDbd-P3uH0mAbXf36SbPBDNOkJjaFzCYcGz68uZ7cnePbz4voEG19PZBvxg4ltGBNemTh4F9N7tN2YLrnDzXmAfny7uD2fFfOby6vzr_PClkoNBZdWcdGUlJq6bFRT2Uo6ZaBWsGgEdVVtnWXSSMGFUaQ0qraULZwCWgsOjB2gL2vf1bjoXaanyJ1exbY38VEH0-q_Fd_e6WV40FQKoSjNBscbgxh-jS4Num-TdV1nvMsDacmYYBTKMpOf_ktSQhiVRGbw4xvwPozR5zVkRlHFVUUyRNaQjSGl6JrnzAT0VLZel61z2XoqW08JPrwe9uXFpt0M0DWQsuSXLr78_G_X36JntVI</recordid><startdate>20090701</startdate><enddate>20090701</enddate><creator>Steinberg, Marcos W.</creator><creator>Shui, Jr-Wen</creator><creator>Ware, Carl F.</creator><creator>Kronenberg, Mitchell</creator><general>Springer-Verlag</general><general>Springer Nature B.V</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>7U9</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090701</creationdate><title>Regulating the mucosal immune system: the contrasting roles of LIGHT, HVEM, and their various partners</title><author>Steinberg, Marcos W. ; Shui, Jr-Wen ; Ware, Carl F. ; Kronenberg, Mitchell</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-57c956f422ad4f9f8c87e9a0d90bf62e8dcec37a7656a914a9dc23be902d65033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Antigens</topic><topic>B-Lymphocytes - immunology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cytokines</topic><topic>Glycoproteins</topic><topic>Herpes simplex</topic><topic>Herpes viruses</topic><topic>Herpesvirus</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunity, Mucosal</topic><topic>Immunoglobulins</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Inflammation - immunology</topic><topic>Inflammatory bowel disease</topic><topic>Internal Medicine</topic><topic>Intestinal Mucosa - immunology</topic><topic>Intestine</topic><topic>Ligands</topic><topic>Light</topic><topic>LIGHT protein</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Lymphotoxin</topic><topic>Mucosal immunity</topic><topic>Pathogenesis</topic><topic>Receptors, Tumor Necrosis Factor, Member 14 - immunology</topic><topic>Review</topic><topic>Signal transduction</topic><topic>T-Lymphocytes - immunology</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor Ligand Superfamily Member 14 - immunology</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Steinberg, Marcos W.</creatorcontrib><creatorcontrib>Shui, Jr-Wen</creatorcontrib><creatorcontrib>Ware, Carl F.</creatorcontrib><creatorcontrib>Kronenberg, Mitchell</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><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 Pharma Collection</collection><collection>Public Health Database</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>Virology and AIDS Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Seminars in immunopathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Steinberg, Marcos W.</au><au>Shui, Jr-Wen</au><au>Ware, Carl F.</au><au>Kronenberg, Mitchell</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulating the mucosal immune system: the contrasting roles of LIGHT, HVEM, and their various partners</atitle><jtitle>Seminars in immunopathology</jtitle><stitle>Semin Immunopathol</stitle><addtitle>Semin Immunopathol</addtitle><date>2009-07-01</date><risdate>2009</risdate><volume>31</volume><issue>2</issue><spage>207</spage><epage>221</epage><pages>207-221</pages><issn>1863-2297</issn><eissn>1863-2300</eissn><abstract>LIGHT and herpes virus entry mediator (HVEM) comprise a ligand–receptor pair in the tumor necrosis factor superfamily. These molecules play an important role in regulating immunity, particularly in the intestinal mucosa. LIGHT also binds the lymphotoxin β receptor, and HVEM can act as a ligand for immunoglobulin family molecules, including B- and T-lymphocyte attenuator, which suppresses immune responses. Complexity in this pivotal system arises from several factors, including the non-monogamous pairing of ligands and receptors, and reverse signaling or the ability of some ligands to serve as receptors. As a result, recognition events in this fascinating network of interacting molecules can have pro- or anti-inflammatory consequences. Despite complexity, experiments we and others are carrying out are establishing rules for understanding when and in what cell types these molecules contribute to intestinal inflammation.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>19495760</pmid><doi>10.1007/s00281-009-0157-4</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antigens B-Lymphocytes - immunology Biomedical and Life Sciences Biomedicine Cytokines Glycoproteins Herpes simplex Herpes viruses Herpesvirus Humans Immune response Immune system Immunity, Mucosal Immunoglobulins Immunology Inflammation Inflammation - immunology Inflammatory bowel disease Internal Medicine Intestinal Mucosa - immunology Intestine Ligands Light LIGHT protein Lymphocytes Lymphocytes T Lymphotoxin Mucosal immunity Pathogenesis Receptors, Tumor Necrosis Factor, Member 14 - immunology Review Signal transduction T-Lymphocytes - immunology Tumor necrosis factor Tumor Necrosis Factor Ligand Superfamily Member 14 - immunology Tumor necrosis factor-TNF |
title | Regulating the mucosal immune system: the contrasting roles of LIGHT, HVEM, and their various partners |
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