The emergence of the IL‐36 cytokine family as novel targets for inflammatory diseases
The recently discovered interleukin (IL)‐36 family of cytokines form part of the broader IL‐1 family and are emerging as important mediators of inflammatory disease. The IL‐36 subfamily consists of three ligands—IL‐36α, IL‐36β, and IL‐36γ—and the natural antagonist IL‐36Ra. The cytokines exert their...
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| Veröffentlicht in: | Annals of the New York Academy of Sciences 2018-04, Vol.1417 (1), p.23-34 |
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| creator | Walsh, Patrick T. Fallon, Padraic G. |
| description | The recently discovered interleukin (IL)‐36 family of cytokines form part of the broader IL‐1 family and are emerging as important mediators of inflammatory disease. The IL‐36 subfamily consists of three ligands—IL‐36α, IL‐36β, and IL‐36γ—and the natural antagonist IL‐36Ra. The cytokines exert their effects through a specific IL‐36 receptor consisting of IL‐36R and IL‐1RAcP chains. IL‐36 cytokines can direct both innate and adaptive immune responses by acting on parenchymal, stromal, and specific immune cell subsets. In humans, inactivating mutations in the gene encoding the IL‐36R antagonist, which lead to unregulated IL‐36R signaling, lead to an autoinflammatory condition termed deficiency of the IL‐36R antagonist, which primarily manifests as a severe form of pustular psoriasis. While such discoveries have prompted deeper mechanistic studies highlighting the important role of IL‐36 cytokines in psoriatic skin inflammation, it is now evident that IL‐36 cytokines can also play important roles in inflammatory disorders in other organs, such as the gastrointestinal tract and the lungs. Given these emerging roles, strategies to specifically target the expression and activity of the IL‐36 family have the potential to uncover novel therapeutic approaches aimed at treating inflammatory diseases in humans. |
| doi_str_mv | 10.1111/nyas.13280 |
| format | Article |
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The IL‐36 subfamily consists of three ligands—IL‐36α, IL‐36β, and IL‐36γ—and the natural antagonist IL‐36Ra. The cytokines exert their effects through a specific IL‐36 receptor consisting of IL‐36R and IL‐1RAcP chains. IL‐36 cytokines can direct both innate and adaptive immune responses by acting on parenchymal, stromal, and specific immune cell subsets. In humans, inactivating mutations in the gene encoding the IL‐36R antagonist, which lead to unregulated IL‐36R signaling, lead to an autoinflammatory condition termed deficiency of the IL‐36R antagonist, which primarily manifests as a severe form of pustular psoriasis. While such discoveries have prompted deeper mechanistic studies highlighting the important role of IL‐36 cytokines in psoriatic skin inflammation, it is now evident that IL‐36 cytokines can also play important roles in inflammatory disorders in other organs, such as the gastrointestinal tract and the lungs. Given these emerging roles, strategies to specifically target the expression and activity of the IL‐36 family have the potential to uncover novel therapeutic approaches aimed at treating inflammatory diseases in humans.</description><identifier>ISSN: 0077-8923</identifier><identifier>EISSN: 1749-6632</identifier><identifier>DOI: 10.1111/nyas.13280</identifier><identifier>PMID: 27783881</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Adaptive immunity ; Cytokines ; Gastrointestinal tract ; Gene Expression ; Humans ; Immune response ; inflammation ; Inflammation - genetics ; Inflammation - immunology ; Inflammation Mediators - immunology ; inflammatory bowel disease ; Inflammatory Bowel Diseases - genetics ; Inflammatory Bowel Diseases - immunology ; Inflammatory diseases ; Interleukin-1 - chemistry ; Interleukin-1 - genetics ; Interleukin-1 - immunology ; Interleukins ; Interleukins - chemistry ; Interleukins - genetics ; Interleukins - immunology ; interleukin‐36 ; Lungs ; Models, Immunological ; Mutation ; Organs ; Psoriasis ; Psoriasis - genetics ; Psoriasis - immunology ; Skin ; Skin diseases</subject><ispartof>Annals of the New York Academy of Sciences, 2018-04, Vol.1417 (1), p.23-34</ispartof><rights>2016 New York Academy of Sciences.</rights><rights>2018 The New York Academy of Sciences</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4230-80a8a65e54aa1220db0a88a1912a43f27e10fcfb525f92991cbb582b691e02443</citedby><cites>FETCH-LOGICAL-c4230-80a8a65e54aa1220db0a88a1912a43f27e10fcfb525f92991cbb582b691e02443</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fnyas.13280$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fnyas.13280$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27783881$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Walsh, Patrick T.</creatorcontrib><creatorcontrib>Fallon, Padraic G.</creatorcontrib><title>The emergence of the IL‐36 cytokine family as novel targets for inflammatory diseases</title><title>Annals of the New York Academy of Sciences</title><addtitle>Ann N Y Acad Sci</addtitle><description>The recently discovered interleukin (IL)‐36 family of cytokines form part of the broader IL‐1 family and are emerging as important mediators of inflammatory disease. The IL‐36 subfamily consists of three ligands—IL‐36α, IL‐36β, and IL‐36γ—and the natural antagonist IL‐36Ra. The cytokines exert their effects through a specific IL‐36 receptor consisting of IL‐36R and IL‐1RAcP chains. IL‐36 cytokines can direct both innate and adaptive immune responses by acting on parenchymal, stromal, and specific immune cell subsets. In humans, inactivating mutations in the gene encoding the IL‐36R antagonist, which lead to unregulated IL‐36R signaling, lead to an autoinflammatory condition termed deficiency of the IL‐36R antagonist, which primarily manifests as a severe form of pustular psoriasis. While such discoveries have prompted deeper mechanistic studies highlighting the important role of IL‐36 cytokines in psoriatic skin inflammation, it is now evident that IL‐36 cytokines can also play important roles in inflammatory disorders in other organs, such as the gastrointestinal tract and the lungs. Given these emerging roles, strategies to specifically target the expression and activity of the IL‐36 family have the potential to uncover novel therapeutic approaches aimed at treating inflammatory diseases in humans.</description><subject>Adaptive immunity</subject><subject>Cytokines</subject><subject>Gastrointestinal tract</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>Immune response</subject><subject>inflammation</subject><subject>Inflammation - genetics</subject><subject>Inflammation - immunology</subject><subject>Inflammation Mediators - immunology</subject><subject>inflammatory bowel disease</subject><subject>Inflammatory Bowel Diseases - genetics</subject><subject>Inflammatory Bowel Diseases - immunology</subject><subject>Inflammatory diseases</subject><subject>Interleukin-1 - chemistry</subject><subject>Interleukin-1 - genetics</subject><subject>Interleukin-1 - immunology</subject><subject>Interleukins</subject><subject>Interleukins - chemistry</subject><subject>Interleukins - genetics</subject><subject>Interleukins - immunology</subject><subject>interleukin‐36</subject><subject>Lungs</subject><subject>Models, Immunological</subject><subject>Mutation</subject><subject>Organs</subject><subject>Psoriasis</subject><subject>Psoriasis - genetics</subject><subject>Psoriasis - immunology</subject><subject>Skin</subject><subject>Skin diseases</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtKxDAUhoMoOl42PoAE3IjQMZemSZcyeINBF46Iq5B2TrTaNpp0lO58BJ_RJzHjjC5ceDYHfr7zc_gQ2qVkSOMctb0JQ8qZIitoQGWaJ1nG2SoaECJlonLGN9BmCI-EUKZSuY42mJSKK0UH6HbyABga8PfQloCdxV0MLsaf7x88w2XfuaeqBWxNU9U9NgG37hVq3Jl40AVsncdVa2vTNKZzvsfTKoAJELbRmjV1gJ3l3kI3pyeT0Xkyvjq7GB2PkzJlnCSKGGUyASI1hjJGpkUMlKE5ZSbllkmgxJa2EEzYnOU5LYtCKFZkOQXC0pRvoYNF77N3LzMInW6qUEJdmxbcLGiquMgUZ0JEdP8P-uhmvo3faUY4z5SkqYzU4YIqvQvBg9XPvmqM7zUleq5bz3Xrb90R3ltWzooGpr_oj98I0AXwVtXQ_1OlL--OrxelX28bidg</recordid><startdate>201804</startdate><enddate>201804</enddate><creator>Walsh, Patrick T.</creator><creator>Fallon, Padraic G.</creator><general>Wiley Subscription Services, Inc</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7ST</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>SOI</scope><scope>7X8</scope></search><sort><creationdate>201804</creationdate><title>The emergence of the IL‐36 cytokine family as novel targets for inflammatory diseases</title><author>Walsh, Patrick T. ; Fallon, Padraic G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4230-80a8a65e54aa1220db0a88a1912a43f27e10fcfb525f92991cbb582b691e02443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adaptive immunity</topic><topic>Cytokines</topic><topic>Gastrointestinal tract</topic><topic>Gene Expression</topic><topic>Humans</topic><topic>Immune response</topic><topic>inflammation</topic><topic>Inflammation - genetics</topic><topic>Inflammation - immunology</topic><topic>Inflammation Mediators - immunology</topic><topic>inflammatory bowel disease</topic><topic>Inflammatory Bowel Diseases - genetics</topic><topic>Inflammatory Bowel Diseases - immunology</topic><topic>Inflammatory diseases</topic><topic>Interleukin-1 - chemistry</topic><topic>Interleukin-1 - genetics</topic><topic>Interleukin-1 - immunology</topic><topic>Interleukins</topic><topic>Interleukins - chemistry</topic><topic>Interleukins - genetics</topic><topic>Interleukins - immunology</topic><topic>interleukin‐36</topic><topic>Lungs</topic><topic>Models, Immunological</topic><topic>Mutation</topic><topic>Organs</topic><topic>Psoriasis</topic><topic>Psoriasis - genetics</topic><topic>Psoriasis - immunology</topic><topic>Skin</topic><topic>Skin diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Walsh, Patrick T.</creatorcontrib><creatorcontrib>Fallon, Padraic G.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Environment Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of the New York Academy of Sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Walsh, Patrick T.</au><au>Fallon, Padraic G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The emergence of the IL‐36 cytokine family as novel targets for inflammatory diseases</atitle><jtitle>Annals of the New York Academy of Sciences</jtitle><addtitle>Ann N Y Acad Sci</addtitle><date>2018-04</date><risdate>2018</risdate><volume>1417</volume><issue>1</issue><spage>23</spage><epage>34</epage><pages>23-34</pages><issn>0077-8923</issn><eissn>1749-6632</eissn><abstract>The recently discovered interleukin (IL)‐36 family of cytokines form part of the broader IL‐1 family and are emerging as important mediators of inflammatory disease. The IL‐36 subfamily consists of three ligands—IL‐36α, IL‐36β, and IL‐36γ—and the natural antagonist IL‐36Ra. The cytokines exert their effects through a specific IL‐36 receptor consisting of IL‐36R and IL‐1RAcP chains. IL‐36 cytokines can direct both innate and adaptive immune responses by acting on parenchymal, stromal, and specific immune cell subsets. In humans, inactivating mutations in the gene encoding the IL‐36R antagonist, which lead to unregulated IL‐36R signaling, lead to an autoinflammatory condition termed deficiency of the IL‐36R antagonist, which primarily manifests as a severe form of pustular psoriasis. While such discoveries have prompted deeper mechanistic studies highlighting the important role of IL‐36 cytokines in psoriatic skin inflammation, it is now evident that IL‐36 cytokines can also play important roles in inflammatory disorders in other organs, such as the gastrointestinal tract and the lungs. 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| subjects | Adaptive immunity Cytokines Gastrointestinal tract Gene Expression Humans Immune response inflammation Inflammation - genetics Inflammation - immunology Inflammation Mediators - immunology inflammatory bowel disease Inflammatory Bowel Diseases - genetics Inflammatory Bowel Diseases - immunology Inflammatory diseases Interleukin-1 - chemistry Interleukin-1 - genetics Interleukin-1 - immunology Interleukins Interleukins - chemistry Interleukins - genetics Interleukins - immunology interleukin‐36 Lungs Models, Immunological Mutation Organs Psoriasis Psoriasis - genetics Psoriasis - immunology Skin Skin diseases |
| title | The emergence of the IL‐36 cytokine family as novel targets for inflammatory diseases |
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