PPARγ enhances ILC2 function during allergic airway inflammation via transcription regulation of ST2
Group 2 innate lymphoid cells (ILC2s) represent the major player during hyperresponsive airway inflammation. Peroxisome proliferator-activated receptor-γ (PPARγ) was highly expressed on ILC2 and its potential role in asthma has been suggested. However, the detailed mechanism underlying the effects o...
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| Veröffentlicht in: | Mucosal immunology 2021-03, Vol.14 (2), p.468-478 |
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| creator | Xiao, Qiang He, Juan Lei, Aihua Xu, Haixu Zhang, Lijuan Zhou, Pan Jiang, Guanmin Zhou, Jie |
| description | Group 2 innate lymphoid cells (ILC2s) represent the major player during hyperresponsive airway inflammation. Peroxisome proliferator-activated receptor-γ (PPARγ) was highly expressed on ILC2 and its potential role in asthma has been suggested. However, the detailed mechanism underlying the effects of PPARγ on ILC2-induced airway inflammation remains to be fully understood. Here we identified PPARγ as a positive regulator of lung ILC2. Expression of PPARγ on ILC2 was dramatically induced upon interleukin-33 (IL-33) challenge. Deficiency of PPARγ in hematopoietic system in mice (PPARγ
fl/fl
Vav1
Cre
) significantly impaired the function of ILC2 in lung, which led to apparent alleviation of airway inflammation in response to IL-33 or Papain challenge, when compared with those in PPARγ
fl/fl
littermates control. Mechanistic studies identified IL-33 receptor ST2 as a transcriptional target of PPARγ. Overexpression of ST2 rescued the functional defects of ILC2 lacking PPARγ. Collectively, these results demonstrated PPARγ as an important regulator of ILC2 during allergic airway inflammation, which sheds new lights on the importance of PPARγ in asthma. |
| doi_str_mv | 10.1038/s41385-020-00339-6 |
| format | Article |
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fl/fl
Vav1
Cre
) significantly impaired the function of ILC2 in lung, which led to apparent alleviation of airway inflammation in response to IL-33 or Papain challenge, when compared with those in PPARγ
fl/fl
littermates control. Mechanistic studies identified IL-33 receptor ST2 as a transcriptional target of PPARγ. Overexpression of ST2 rescued the functional defects of ILC2 lacking PPARγ. Collectively, these results demonstrated PPARγ as an important regulator of ILC2 during allergic airway inflammation, which sheds new lights on the importance of PPARγ in asthma.</description><identifier>ISSN: 1933-0219</identifier><identifier>EISSN: 1935-3456</identifier><identifier>DOI: 10.1038/s41385-020-00339-6</identifier><identifier>PMID: 32811992</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Allergology ; Animals ; Antibodies ; Asthma ; Asthma - immunology ; Biomedical and Life Sciences ; Biomedicine ; Cells, Cultured ; Cytokines - metabolism ; Gastroenterology ; Gene Expression Regulation ; Gene regulation ; Humans ; Hypersensitivity - immunology ; Immunity, Innate ; Immunology ; Inflammation ; Inflammation - immunology ; Interleukin-1 Receptor-Like 1 Protein - genetics ; Interleukin-1 Receptor-Like 1 Protein - metabolism ; Lymphocytes - immunology ; Lymphoid cells ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Knockout ; Papain ; PPAR gamma - genetics ; PPAR gamma - metabolism ; Respiratory System - immunology ; Respiratory tract ; Respiratory tract diseases ; Th2 Cells - immunology ; Transcription</subject><ispartof>Mucosal immunology, 2021-03, Vol.14 (2), p.468-478</ispartof><rights>Society for Mucosal Immunology 2020</rights><rights>Society for Mucosal Immunology 2020.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-99fbac9376ea8eccef6841f7d8bbe15a43ca6479a1f991d44d39c201cca070503</citedby><cites>FETCH-LOGICAL-c419t-99fbac9376ea8eccef6841f7d8bbe15a43ca6479a1f991d44d39c201cca070503</cites><orcidid>0000-0001-5964-1599</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32811992$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiao, Qiang</creatorcontrib><creatorcontrib>He, Juan</creatorcontrib><creatorcontrib>Lei, Aihua</creatorcontrib><creatorcontrib>Xu, Haixu</creatorcontrib><creatorcontrib>Zhang, Lijuan</creatorcontrib><creatorcontrib>Zhou, Pan</creatorcontrib><creatorcontrib>Jiang, Guanmin</creatorcontrib><creatorcontrib>Zhou, Jie</creatorcontrib><title>PPARγ enhances ILC2 function during allergic airway inflammation via transcription regulation of ST2</title><title>Mucosal immunology</title><addtitle>Mucosal Immunol</addtitle><addtitle>Mucosal Immunol</addtitle><description>Group 2 innate lymphoid cells (ILC2s) represent the major player during hyperresponsive airway inflammation. Peroxisome proliferator-activated receptor-γ (PPARγ) was highly expressed on ILC2 and its potential role in asthma has been suggested. However, the detailed mechanism underlying the effects of PPARγ on ILC2-induced airway inflammation remains to be fully understood. Here we identified PPARγ as a positive regulator of lung ILC2. Expression of PPARγ on ILC2 was dramatically induced upon interleukin-33 (IL-33) challenge. Deficiency of PPARγ in hematopoietic system in mice (PPARγ
fl/fl
Vav1
Cre
) significantly impaired the function of ILC2 in lung, which led to apparent alleviation of airway inflammation in response to IL-33 or Papain challenge, when compared with those in PPARγ
fl/fl
littermates control. Mechanistic studies identified IL-33 receptor ST2 as a transcriptional target of PPARγ. Overexpression of ST2 rescued the functional defects of ILC2 lacking PPARγ. Collectively, these results demonstrated PPARγ as an important regulator of ILC2 during allergic airway inflammation, which sheds new lights on the importance of PPARγ in asthma.</description><subject>Allergology</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Asthma</subject><subject>Asthma - immunology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cells, Cultured</subject><subject>Cytokines - metabolism</subject><subject>Gastroenterology</subject><subject>Gene Expression Regulation</subject><subject>Gene regulation</subject><subject>Humans</subject><subject>Hypersensitivity - immunology</subject><subject>Immunity, Innate</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Inflammation - immunology</subject><subject>Interleukin-1 Receptor-Like 1 Protein - genetics</subject><subject>Interleukin-1 Receptor-Like 1 Protein - metabolism</subject><subject>Lymphocytes - immunology</subject><subject>Lymphoid cells</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred NOD</subject><subject>Mice, Knockout</subject><subject>Papain</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>Respiratory System - immunology</subject><subject>Respiratory tract</subject><subject>Respiratory tract diseases</subject><subject>Th2 Cells - immunology</subject><subject>Transcription</subject><issn>1933-0219</issn><issn>1935-3456</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kcFO3DAQhq0KxFLKC3CoLHHpJcWO7SRzRCtKV1qpCLZna9axt0aJs9gbEM_Fe_BMZDdbKvXAaUYz3_wzmp-QM86-cyaqiyS5qFTGcpYxJgRkxSdyzEGoTEhVHOxyMbQ5TMjnlO4ZKxhT4ohMRF5xDpAfE3tzc3n7-kJt-IPB2ERn82lOXR_MxneB1n30YUWxaWxceUPRxyd8pj64BtsWd8yjR7qJGJKJfr2rRLvqm7HZOXq3yL-QQ4dNsqf7eEJ-_7haTH9m81_Xs-nlPDOSwyYDcEs0IMrCYmWNsa6oJHdlXS2XliuUwmAhS0DuAHgtZS3A5Iwbg6xkiokT8m3UXcfuobdpo1ufjG0aDLbrk86lUEpwXm7R8__Q-66PYbhuoAAKBWUFA5WPlIldStE6vY6-xfisOdNbE_Rogh5M0DsTdDEMfd1L98vW1u8jf78-AGIE0nr7Xhv_7f5A9g0A-JLs</recordid><startdate>20210301</startdate><enddate>20210301</enddate><creator>Xiao, Qiang</creator><creator>He, Juan</creator><creator>Lei, Aihua</creator><creator>Xu, Haixu</creator><creator>Zhang, Lijuan</creator><creator>Zhou, Pan</creator><creator>Jiang, Guanmin</creator><creator>Zhou, Jie</creator><general>Nature Publishing Group US</general><general>Elsevier Limited</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>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><orcidid>https://orcid.org/0000-0001-5964-1599</orcidid></search><sort><creationdate>20210301</creationdate><title>PPARγ enhances ILC2 function during allergic airway inflammation via transcription regulation of ST2</title><author>Xiao, Qiang ; He, Juan ; Lei, Aihua ; Xu, Haixu ; Zhang, Lijuan ; Zhou, Pan ; Jiang, Guanmin ; Zhou, Jie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-99fbac9376ea8eccef6841f7d8bbe15a43ca6479a1f991d44d39c201cca070503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Allergology</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Asthma</topic><topic>Asthma - immunology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cells, Cultured</topic><topic>Cytokines - metabolism</topic><topic>Gastroenterology</topic><topic>Gene Expression Regulation</topic><topic>Gene regulation</topic><topic>Humans</topic><topic>Hypersensitivity - immunology</topic><topic>Immunity, Innate</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Inflammation - immunology</topic><topic>Interleukin-1 Receptor-Like 1 Protein - genetics</topic><topic>Interleukin-1 Receptor-Like 1 Protein - metabolism</topic><topic>Lymphocytes - immunology</topic><topic>Lymphoid cells</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred NOD</topic><topic>Mice, Knockout</topic><topic>Papain</topic><topic>PPAR gamma - genetics</topic><topic>PPAR gamma - metabolism</topic><topic>Respiratory System - immunology</topic><topic>Respiratory tract</topic><topic>Respiratory tract diseases</topic><topic>Th2 Cells - immunology</topic><topic>Transcription</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiao, Qiang</creatorcontrib><creatorcontrib>He, Juan</creatorcontrib><creatorcontrib>Lei, Aihua</creatorcontrib><creatorcontrib>Xu, Haixu</creatorcontrib><creatorcontrib>Zhang, Lijuan</creatorcontrib><creatorcontrib>Zhou, Pan</creatorcontrib><creatorcontrib>Jiang, Guanmin</creatorcontrib><creatorcontrib>Zhou, Jie</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 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>Xiao, Qiang</au><au>He, Juan</au><au>Lei, Aihua</au><au>Xu, Haixu</au><au>Zhang, Lijuan</au><au>Zhou, Pan</au><au>Jiang, Guanmin</au><au>Zhou, Jie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PPARγ enhances ILC2 function during allergic airway inflammation via transcription regulation of ST2</atitle><jtitle>Mucosal immunology</jtitle><stitle>Mucosal Immunol</stitle><addtitle>Mucosal Immunol</addtitle><date>2021-03-01</date><risdate>2021</risdate><volume>14</volume><issue>2</issue><spage>468</spage><epage>478</epage><pages>468-478</pages><issn>1933-0219</issn><eissn>1935-3456</eissn><abstract>Group 2 innate lymphoid cells (ILC2s) represent the major player during hyperresponsive airway inflammation. Peroxisome proliferator-activated receptor-γ (PPARγ) was highly expressed on ILC2 and its potential role in asthma has been suggested. However, the detailed mechanism underlying the effects of PPARγ on ILC2-induced airway inflammation remains to be fully understood. Here we identified PPARγ as a positive regulator of lung ILC2. Expression of PPARγ on ILC2 was dramatically induced upon interleukin-33 (IL-33) challenge. Deficiency of PPARγ in hematopoietic system in mice (PPARγ
fl/fl
Vav1
Cre
) significantly impaired the function of ILC2 in lung, which led to apparent alleviation of airway inflammation in response to IL-33 or Papain challenge, when compared with those in PPARγ
fl/fl
littermates control. Mechanistic studies identified IL-33 receptor ST2 as a transcriptional target of PPARγ. Overexpression of ST2 rescued the functional defects of ILC2 lacking PPARγ. Collectively, these results demonstrated PPARγ as an important regulator of ILC2 during allergic airway inflammation, which sheds new lights on the importance of PPARγ in asthma.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>32811992</pmid><doi>10.1038/s41385-020-00339-6</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-5964-1599</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Mucosal immunology, 2021-03, Vol.14 (2), p.468-478 |
| issn | 1933-0219 1935-3456 |
| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Allergology Animals Antibodies Asthma Asthma - immunology Biomedical and Life Sciences Biomedicine Cells, Cultured Cytokines - metabolism Gastroenterology Gene Expression Regulation Gene regulation Humans Hypersensitivity - immunology Immunity, Innate Immunology Inflammation Inflammation - immunology Interleukin-1 Receptor-Like 1 Protein - genetics Interleukin-1 Receptor-Like 1 Protein - metabolism Lymphocytes - immunology Lymphoid cells Mice Mice, Inbred C57BL Mice, Inbred NOD Mice, Knockout Papain PPAR gamma - genetics PPAR gamma - metabolism Respiratory System - immunology Respiratory tract Respiratory tract diseases Th2 Cells - immunology Transcription |
| title | PPARγ enhances ILC2 function during allergic airway inflammation via transcription regulation of ST2 |
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