IL-1 is a critical regulator of group 2 innate lymphoid cell function and plasticity
Cytokines of the IL-1 family have a range of effects on innate lymphoid cells. Liu and colleagues find that IL-1 facilitates the maturation and plasticity of group 2 innate lymphoid cells. Group 2 innate lymphoid cells (ILC2 cells) are important for type 2 immune responses and are activated by the e...
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Veröffentlicht in: | Nature immunology 2016-06, Vol.17 (6), p.646-655 |
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creator | Ohne, Yoichiro Silver, Jonathan S Thompson-Snipes, LuAnn Collet, Magalie A Blanck, Jean Philippe Cantarel, Brandi L Copenhaver, Alan M Humbles, Alison A Liu, Yong-Jun |
description | Cytokines of the IL-1 family have a range of effects on innate lymphoid cells. Liu and colleagues find that IL-1 facilitates the maturation and plasticity of group 2 innate lymphoid cells.
Group 2 innate lymphoid cells (ILC2 cells) are important for type 2 immune responses and are activated by the epithelial cytokines interleukin 33 (IL-33), IL-25 and thymic stromal lymphopoietin (TSLP). Here we demonstrated that IL-1β was a critical activator of ILC2 cells, inducing proliferation and cytokine production and regulating the expression of epithelial cytokine receptors. IL-1β also governed ILC2 plasticity by inducing low expression of the transcription factor T-bet and the cytokine receptor chain IL-12Rβ2, which enabled the conversion of these cells into an ILC1 phenotype in response to IL-12. This transition was marked by an atypical chromatin landscape characterized by the simultaneous transcriptional accessibility of the locus encoding interferon-γ (IFN-γ) and the loci encoding IL-5 and IL-13. Finally, IL-1β potentiated ILC2 activation and plasticity
in vivo
, and IL-12 acted as the switch that determined an ILC2-versus-ILC1 response. Thus, we have identified a previously unknown role for IL-1β in facilitating ILC2 maturation and plasticity. |
doi_str_mv | 10.1038/ni.3447 |
format | Article |
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Group 2 innate lymphoid cells (ILC2 cells) are important for type 2 immune responses and are activated by the epithelial cytokines interleukin 33 (IL-33), IL-25 and thymic stromal lymphopoietin (TSLP). Here we demonstrated that IL-1β was a critical activator of ILC2 cells, inducing proliferation and cytokine production and regulating the expression of epithelial cytokine receptors. IL-1β also governed ILC2 plasticity by inducing low expression of the transcription factor T-bet and the cytokine receptor chain IL-12Rβ2, which enabled the conversion of these cells into an ILC1 phenotype in response to IL-12. This transition was marked by an atypical chromatin landscape characterized by the simultaneous transcriptional accessibility of the locus encoding interferon-γ (IFN-γ) and the loci encoding IL-5 and IL-13. Finally, IL-1β potentiated ILC2 activation and plasticity
in vivo
, and IL-12 acted as the switch that determined an ILC2-versus-ILC1 response. Thus, we have identified a previously unknown role for IL-1β in facilitating ILC2 maturation and plasticity.</description><identifier>ISSN: 1529-2908</identifier><identifier>EISSN: 1529-2916</identifier><identifier>DOI: 10.1038/ni.3447</identifier><identifier>PMID: 27111142</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>13/106 ; 13/31 ; 38/39 ; 45/91 ; 631/250/127/1213 ; 631/250/2504/2506 ; Animals ; Biomedicine ; Cell Differentiation ; Cell Plasticity - immunology ; Cells, Cultured ; Cytokines - metabolism ; Humans ; Immunity, Innate ; Immunology ; Infectious Diseases ; Interferon-gamma - metabolism ; Interleukin-1 ; Interleukin-12 - metabolism ; Interleukin-17 - metabolism ; Interleukin-1beta - metabolism ; Interleukin-33 - metabolism ; Lymphocytes - immunology ; Lymphoid tissue ; Mice ; Mice, SCID ; Phenotypic plasticity ; Physiological aspects ; Plasticity ; Receptors, Interleukin-12 - genetics ; Receptors, Interleukin-12 - metabolism ; Signal Transduction ; T-Box Domain Proteins - genetics ; T-Box Domain Proteins - metabolism ; Th1 Cells - immunology ; Th1-Th2 Balance ; Th2 Cells - immunology</subject><ispartof>Nature immunology, 2016-06, Vol.17 (6), p.646-655</ispartof><rights>Springer Nature America, Inc. 2016</rights><rights>COPYRIGHT 2016 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jun 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c542t-a236fb40139b66190c39291fbe4e4783f5af1c17b3f29ac9a0d7e4b4460f5f693</citedby><cites>FETCH-LOGICAL-c542t-a236fb40139b66190c39291fbe4e4783f5af1c17b3f29ac9a0d7e4b4460f5f693</cites><orcidid>0000-0003-4126-4478</orcidid></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.3447$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ni.3447$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27911,27912,41475,42544,51306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27111142$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ohne, Yoichiro</creatorcontrib><creatorcontrib>Silver, Jonathan S</creatorcontrib><creatorcontrib>Thompson-Snipes, LuAnn</creatorcontrib><creatorcontrib>Collet, Magalie A</creatorcontrib><creatorcontrib>Blanck, Jean Philippe</creatorcontrib><creatorcontrib>Cantarel, Brandi L</creatorcontrib><creatorcontrib>Copenhaver, Alan M</creatorcontrib><creatorcontrib>Humbles, Alison A</creatorcontrib><creatorcontrib>Liu, Yong-Jun</creatorcontrib><title>IL-1 is a critical regulator of group 2 innate lymphoid cell function and plasticity</title><title>Nature immunology</title><addtitle>Nat Immunol</addtitle><addtitle>Nat Immunol</addtitle><description>Cytokines of the IL-1 family have a range of effects on innate lymphoid cells. Liu and colleagues find that IL-1 facilitates the maturation and plasticity of group 2 innate lymphoid cells.
Group 2 innate lymphoid cells (ILC2 cells) are important for type 2 immune responses and are activated by the epithelial cytokines interleukin 33 (IL-33), IL-25 and thymic stromal lymphopoietin (TSLP). Here we demonstrated that IL-1β was a critical activator of ILC2 cells, inducing proliferation and cytokine production and regulating the expression of epithelial cytokine receptors. IL-1β also governed ILC2 plasticity by inducing low expression of the transcription factor T-bet and the cytokine receptor chain IL-12Rβ2, which enabled the conversion of these cells into an ILC1 phenotype in response to IL-12. This transition was marked by an atypical chromatin landscape characterized by the simultaneous transcriptional accessibility of the locus encoding interferon-γ (IFN-γ) and the loci encoding IL-5 and IL-13. Finally, IL-1β potentiated ILC2 activation and plasticity
in vivo
, and IL-12 acted as the switch that determined an ILC2-versus-ILC1 response. Thus, we have identified a previously unknown role for IL-1β in facilitating ILC2 maturation and plasticity.</description><subject>13/106</subject><subject>13/31</subject><subject>38/39</subject><subject>45/91</subject><subject>631/250/127/1213</subject><subject>631/250/2504/2506</subject><subject>Animals</subject><subject>Biomedicine</subject><subject>Cell Differentiation</subject><subject>Cell Plasticity - immunology</subject><subject>Cells, Cultured</subject><subject>Cytokines - metabolism</subject><subject>Humans</subject><subject>Immunity, Innate</subject><subject>Immunology</subject><subject>Infectious Diseases</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-1</subject><subject>Interleukin-12 - metabolism</subject><subject>Interleukin-17 - metabolism</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukin-33 - metabolism</subject><subject>Lymphocytes - immunology</subject><subject>Lymphoid tissue</subject><subject>Mice</subject><subject>Mice, SCID</subject><subject>Phenotypic plasticity</subject><subject>Physiological aspects</subject><subject>Plasticity</subject><subject>Receptors, Interleukin-12 - 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Academic</collection><jtitle>Nature immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ohne, Yoichiro</au><au>Silver, Jonathan S</au><au>Thompson-Snipes, LuAnn</au><au>Collet, Magalie A</au><au>Blanck, Jean Philippe</au><au>Cantarel, Brandi L</au><au>Copenhaver, Alan M</au><au>Humbles, Alison A</au><au>Liu, Yong-Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL-1 is a critical regulator of group 2 innate lymphoid cell function and plasticity</atitle><jtitle>Nature immunology</jtitle><stitle>Nat Immunol</stitle><addtitle>Nat Immunol</addtitle><date>2016-06-01</date><risdate>2016</risdate><volume>17</volume><issue>6</issue><spage>646</spage><epage>655</epage><pages>646-655</pages><issn>1529-2908</issn><eissn>1529-2916</eissn><abstract>Cytokines of the IL-1 family have a range of effects on innate lymphoid cells. Liu and colleagues find that IL-1 facilitates the maturation and plasticity of group 2 innate lymphoid cells.
Group 2 innate lymphoid cells (ILC2 cells) are important for type 2 immune responses and are activated by the epithelial cytokines interleukin 33 (IL-33), IL-25 and thymic stromal lymphopoietin (TSLP). Here we demonstrated that IL-1β was a critical activator of ILC2 cells, inducing proliferation and cytokine production and regulating the expression of epithelial cytokine receptors. IL-1β also governed ILC2 plasticity by inducing low expression of the transcription factor T-bet and the cytokine receptor chain IL-12Rβ2, which enabled the conversion of these cells into an ILC1 phenotype in response to IL-12. This transition was marked by an atypical chromatin landscape characterized by the simultaneous transcriptional accessibility of the locus encoding interferon-γ (IFN-γ) and the loci encoding IL-5 and IL-13. Finally, IL-1β potentiated ILC2 activation and plasticity
in vivo
, and IL-12 acted as the switch that determined an ILC2-versus-ILC1 response. Thus, we have identified a previously unknown role for IL-1β in facilitating ILC2 maturation and plasticity.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>27111142</pmid><doi>10.1038/ni.3447</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-4126-4478</orcidid></addata></record> |
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subjects | 13/106 13/31 38/39 45/91 631/250/127/1213 631/250/2504/2506 Animals Biomedicine Cell Differentiation Cell Plasticity - immunology Cells, Cultured Cytokines - metabolism Humans Immunity, Innate Immunology Infectious Diseases Interferon-gamma - metabolism Interleukin-1 Interleukin-12 - metabolism Interleukin-17 - metabolism Interleukin-1beta - metabolism Interleukin-33 - metabolism Lymphocytes - immunology Lymphoid tissue Mice Mice, SCID Phenotypic plasticity Physiological aspects Plasticity Receptors, Interleukin-12 - genetics Receptors, Interleukin-12 - metabolism Signal Transduction T-Box Domain Proteins - genetics T-Box Domain Proteins - metabolism Th1 Cells - immunology Th1-Th2 Balance Th2 Cells - immunology |
title | IL-1 is a critical regulator of group 2 innate lymphoid cell function and plasticity |
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