NKT cells are required to induce high IL‐33 expression in hepatocytes during ConA‐induced acute hepatitis
Interleukin‐33 (IL‐33) is thought to be released during cellular death as an alarmin cytokine during the acute phase of disease, but its regulation in vivo is poorly understood. We investigated the expression of IL‐33 in two mouse models of acute hepatitis by administering either carbon tetrachlorid...
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| Veröffentlicht in: | European journal of immunology 2011-08, Vol.41 (8), p.2341-2348 |
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| container_title | European journal of immunology |
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| creator | Arshad, Muhammad I. Rauch, Michel L'Helgoualc'h, Annie Julia, Valérie Leite‐de‐Moraes, Maria C. Lucas‐Clerc, Catherine Piquet‐Pellorce, Claire Samson, Michel |
| description | Interleukin‐33 (IL‐33) is thought to be released during cellular death as an alarmin cytokine during the acute phase of disease, but its regulation in vivo is poorly understood. We investigated the expression of IL‐33 in two mouse models of acute hepatitis by administering either carbon tetrachloride (CCl4) or concanavalin A (ConA). IL‐33 was overexpressed in both models but with a stronger induction in ConA‐induced hepatitis. IL‐33 was weakly expressed in vascular and sinusoidal endothelial cells from normal liver and was clearly induced in CCl4‐treated mice. Surprisingly, we found that hepatocytes strongly expressed IL‐33 exclusively in the ConA model. CD1d knock‐out mice, which are deficient in NKT cells and resistant to ConA‐induced hepatitis, no longer expressed IL‐33 in hepatocytes following ConA administration. Interestingly, invariant NKT (iNKT) cells adoptively transferred into ConA‐treated CD1d KO mouse restored IL‐33 expression in hepatocytes. This strongly suggests that NKT cells are responsible for the induction of IL‐33 in hepatocytes. |
| doi_str_mv | 10.1002/eji.201041332 |
| format | Article |
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We investigated the expression of IL‐33 in two mouse models of acute hepatitis by administering either carbon tetrachloride (CCl4) or concanavalin A (ConA). IL‐33 was overexpressed in both models but with a stronger induction in ConA‐induced hepatitis. IL‐33 was weakly expressed in vascular and sinusoidal endothelial cells from normal liver and was clearly induced in CCl4‐treated mice. Surprisingly, we found that hepatocytes strongly expressed IL‐33 exclusively in the ConA model. CD1d knock‐out mice, which are deficient in NKT cells and resistant to ConA‐induced hepatitis, no longer expressed IL‐33 in hepatocytes following ConA administration. Interestingly, invariant NKT (iNKT) cells adoptively transferred into ConA‐treated CD1d KO mouse restored IL‐33 expression in hepatocytes. This strongly suggests that NKT cells are responsible for the induction of IL‐33 in hepatocytes.</description><identifier>ISSN: 0014-2980</identifier><identifier>EISSN: 1521-4141</identifier><identifier>DOI: 10.1002/eji.201041332</identifier><identifier>PMID: 21557213</identifier><identifier>CODEN: EJIMAF</identifier><language>eng</language><publisher>Weinheim: WILEY‐VCH Verlag</publisher><subject>Acute Disease ; Adoptive Transfer ; Alarmin ; Animals ; Antigens, CD1d ; Antigens, CD1d - genetics ; Antigens, CD1d - metabolism ; Carbon Tetrachloride ; Concanavalin A ; Female ; Flow Cytometry ; Fluorescent Antibody Technique ; Gene Expression ; Hepatitis ; Hepatitis, Animal ; Hepatitis, Animal - chemically induced ; Hepatitis, Animal - genetics ; Hepatitis, Animal - metabolism ; Hepatocytes ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; Hepatocytes - pathology ; IL‐33 ; Immunology ; Interleukin-1beta ; Interleukin-1beta - genetics ; Interleukin-1beta - metabolism ; Interleukin-33 ; Interleukin-6 ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Interleukins ; Interleukins - genetics ; Interleukins - metabolism ; Life Sciences ; Liver ; Liver - drug effects ; Liver - metabolism ; Liver - pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Natural Killer T-Cells ; Natural Killer T-Cells - metabolism ; NKT cells ; Reverse Transcriptase Polymerase Chain Reaction ; T cell receptors ; Tumor Necrosis Factor-alpha ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>European journal of immunology, 2011-08, Vol.41 (8), p.2341-2348</ispartof><rights>Copyright © 2011 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim</rights><rights>Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.</rights><rights>Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4742-36315325832f0591ee2ad09b96ae618ed530e383e2c3fc146362d2271cb5750d3</citedby><cites>FETCH-LOGICAL-c4742-36315325832f0591ee2ad09b96ae618ed530e383e2c3fc146362d2271cb5750d3</cites><orcidid>0000-0002-2891-2269</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Feji.201041332$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Feji.201041332$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21557213$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00681990$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Arshad, Muhammad I.</creatorcontrib><creatorcontrib>Rauch, Michel</creatorcontrib><creatorcontrib>L'Helgoualc'h, Annie</creatorcontrib><creatorcontrib>Julia, Valérie</creatorcontrib><creatorcontrib>Leite‐de‐Moraes, Maria C.</creatorcontrib><creatorcontrib>Lucas‐Clerc, Catherine</creatorcontrib><creatorcontrib>Piquet‐Pellorce, Claire</creatorcontrib><creatorcontrib>Samson, Michel</creatorcontrib><title>NKT cells are required to induce high IL‐33 expression in hepatocytes during ConA‐induced acute hepatitis</title><title>European journal of immunology</title><addtitle>Eur J Immunol</addtitle><description>Interleukin‐33 (IL‐33) is thought to be released during cellular death as an alarmin cytokine during the acute phase of disease, but its regulation in vivo is poorly understood. We investigated the expression of IL‐33 in two mouse models of acute hepatitis by administering either carbon tetrachloride (CCl4) or concanavalin A (ConA). IL‐33 was overexpressed in both models but with a stronger induction in ConA‐induced hepatitis. IL‐33 was weakly expressed in vascular and sinusoidal endothelial cells from normal liver and was clearly induced in CCl4‐treated mice. Surprisingly, we found that hepatocytes strongly expressed IL‐33 exclusively in the ConA model. CD1d knock‐out mice, which are deficient in NKT cells and resistant to ConA‐induced hepatitis, no longer expressed IL‐33 in hepatocytes following ConA administration. Interestingly, invariant NKT (iNKT) cells adoptively transferred into ConA‐treated CD1d KO mouse restored IL‐33 expression in hepatocytes. This strongly suggests that NKT cells are responsible for the induction of IL‐33 in hepatocytes.</description><subject>Acute Disease</subject><subject>Adoptive Transfer</subject><subject>Alarmin</subject><subject>Animals</subject><subject>Antigens, CD1d</subject><subject>Antigens, CD1d - genetics</subject><subject>Antigens, CD1d - metabolism</subject><subject>Carbon Tetrachloride</subject><subject>Concanavalin A</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Fluorescent Antibody Technique</subject><subject>Gene Expression</subject><subject>Hepatitis</subject><subject>Hepatitis, Animal</subject><subject>Hepatitis, Animal - chemically induced</subject><subject>Hepatitis, Animal - genetics</subject><subject>Hepatitis, Animal - metabolism</subject><subject>Hepatocytes</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>Hepatocytes - pathology</subject><subject>IL‐33</subject><subject>Immunology</subject><subject>Interleukin-1beta</subject><subject>Interleukin-1beta - genetics</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukin-33</subject><subject>Interleukin-6</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Interleukins</subject><subject>Interleukins - genetics</subject><subject>Interleukins - metabolism</subject><subject>Life Sciences</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>Natural Killer T-Cells</subject><subject>Natural Killer T-Cells - metabolism</subject><subject>NKT cells</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>T cell receptors</subject><subject>Tumor Necrosis Factor-alpha</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0014-2980</issn><issn>1521-4141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90UFv0zAUB3ALgVg3OHJFljgAh4z37DiOj1U1WEcFl3G23OR1dZUmnZ0MeuMj7DPySXCVrUgcdrJk__yX_f6MvUE4RwDxiTb-XABCjlKKZ2yCSmCWY47P2QQA80yYEk7YaYwbADCFMi_ZiUCltEA5YdtvX695RU0TuQvEA90OPlDN-477th4q4mt_s-bzxZ_f91Jy-rULFKPv2nTM17RzfVfte4q8HoJvb_isa6eJjndr7qqhp9H53sdX7MXKNZFeP6xn7Mfni-vZZbb4_mU-my6yKte5yGQhUUmhSilWoAwSCVeDWZrCUYEl1UoCyVKSqOSqwryQhaiF0FgtlVZQyzP2ccxdu8bugt-6sLed8_ZyurCHPYCiRGPgDpN9P9pd6G4Hir3d-niYiGupG6IttSl0qUqT5IcnZRp9noNSeAh99x_ddENo05-TQi1AayWSykZVhS7GQKvjWxHsoV2b2rXHdpN_-5A6LLdUH_VjnQnoEfz0De2fTrMXV_N_0X8BkzOuVQ</recordid><startdate>201108</startdate><enddate>201108</enddate><creator>Arshad, Muhammad I.</creator><creator>Rauch, Michel</creator><creator>L'Helgoualc'h, Annie</creator><creator>Julia, Valérie</creator><creator>Leite‐de‐Moraes, Maria C.</creator><creator>Lucas‐Clerc, Catherine</creator><creator>Piquet‐Pellorce, Claire</creator><creator>Samson, Michel</creator><general>WILEY‐VCH Verlag</general><general>Wiley Subscription Services, Inc</general><general>Wiley-VCH Verlag</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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7U9</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-2891-2269</orcidid></search><sort><creationdate>201108</creationdate><title>NKT cells are required to induce high IL‐33 expression in hepatocytes during ConA‐induced acute hepatitis</title><author>Arshad, Muhammad I. ; 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We investigated the expression of IL‐33 in two mouse models of acute hepatitis by administering either carbon tetrachloride (CCl4) or concanavalin A (ConA). IL‐33 was overexpressed in both models but with a stronger induction in ConA‐induced hepatitis. IL‐33 was weakly expressed in vascular and sinusoidal endothelial cells from normal liver and was clearly induced in CCl4‐treated mice. Surprisingly, we found that hepatocytes strongly expressed IL‐33 exclusively in the ConA model. CD1d knock‐out mice, which are deficient in NKT cells and resistant to ConA‐induced hepatitis, no longer expressed IL‐33 in hepatocytes following ConA administration. Interestingly, invariant NKT (iNKT) cells adoptively transferred into ConA‐treated CD1d KO mouse restored IL‐33 expression in hepatocytes. This strongly suggests that NKT cells are responsible for the induction of IL‐33 in hepatocytes.</abstract><cop>Weinheim</cop><pub>WILEY‐VCH Verlag</pub><pmid>21557213</pmid><doi>10.1002/eji.201041332</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-2891-2269</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Disease Adoptive Transfer Alarmin Animals Antigens, CD1d Antigens, CD1d - genetics Antigens, CD1d - metabolism Carbon Tetrachloride Concanavalin A Female Flow Cytometry Fluorescent Antibody Technique Gene Expression Hepatitis Hepatitis, Animal Hepatitis, Animal - chemically induced Hepatitis, Animal - genetics Hepatitis, Animal - metabolism Hepatocytes Hepatocytes - drug effects Hepatocytes - metabolism Hepatocytes - pathology IL‐33 Immunology Interleukin-1beta Interleukin-1beta - genetics Interleukin-1beta - metabolism Interleukin-33 Interleukin-6 Interleukin-6 - genetics Interleukin-6 - metabolism Interleukins Interleukins - genetics Interleukins - metabolism Life Sciences Liver Liver - drug effects Liver - metabolism Liver - pathology Male Mice Mice, Inbred BALB C Mice, Knockout Natural Killer T-Cells Natural Killer T-Cells - metabolism NKT cells Reverse Transcriptase Polymerase Chain Reaction T cell receptors Tumor Necrosis Factor-alpha Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism |
| title | NKT cells are required to induce high IL‐33 expression in hepatocytes during ConA‐induced acute hepatitis |
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