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Distinct roles of ORAI1 in T cell-mediated allergic airway inflammation and immunity to influenza A virus infection
T cell activation and function depend on Ca signals mediated by store-operated Ca entry (SOCE) through Ca release-activated Ca (CRAC) channels formed by ORAI1 proteins. We here investigated how SOCE controls T cell function in pulmonary inflammation during a T helper 1 (T 1) cell-mediated response t...
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| Published in: | Science advances 2022-10, Vol.8 (40), p.eabn6552-eabn6552 |
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| creator | Wang, Yin-Hu Noyer, Lucile Kahlfuss, Sascha Raphael, Dimitrius Tao, Anthony Y Kaufmann, Ulrike Zhu, Jingjie Mitchell-Flack, Marisa Sidhu, Ikjot Zhou, Fang Vaeth, Martin Thomas, Paul G Saunders, Sean P Stauderman, Kenneth Curotto de Lafaille, Maria A Feske, Stefan |
| description | T cell activation and function depend on Ca
signals mediated by store-operated Ca
entry (SOCE) through Ca
release-activated Ca
(CRAC) channels formed by ORAI1 proteins. We here investigated how SOCE controls T cell function in pulmonary inflammation during a T helper 1 (T
1) cell-mediated response to influenza A virus (IAV) infection and T
2 cell-mediated allergic airway inflammation. T cell-specific deletion of
did not exacerbate pulmonary inflammation and viral burdens following IAV infection but protected mice from house dust mite-induced allergic airway inflammation. ORAI1 controlled the expression of genes including p53 and E2F transcription factors that regulate the cell cycle in T
2 cells in response to allergen stimulation and the expression of transcription factors and cytokines that regulate T
2 cell function. Systemic application of a CRAC channel blocker suppressed allergic airway inflammation without compromising immunity to IAV infection, suggesting that inhibition of SOCE is a potential treatment for allergic airway disease. |
| doi_str_mv | 10.1126/sciadv.abn6552 |
| format | article |
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signals mediated by store-operated Ca
entry (SOCE) through Ca
release-activated Ca
(CRAC) channels formed by ORAI1 proteins. We here investigated how SOCE controls T cell function in pulmonary inflammation during a T helper 1 (T
1) cell-mediated response to influenza A virus (IAV) infection and T
2 cell-mediated allergic airway inflammation. T cell-specific deletion of
did not exacerbate pulmonary inflammation and viral burdens following IAV infection but protected mice from house dust mite-induced allergic airway inflammation. ORAI1 controlled the expression of genes including p53 and E2F transcription factors that regulate the cell cycle in T
2 cells in response to allergen stimulation and the expression of transcription factors and cytokines that regulate T
2 cell function. Systemic application of a CRAC channel blocker suppressed allergic airway inflammation without compromising immunity to IAV infection, suggesting that inhibition of SOCE is a potential treatment for allergic airway disease.</description><identifier>ISSN: 2375-2548</identifier><identifier>EISSN: 2375-2548</identifier><identifier>DOI: 10.1126/sciadv.abn6552</identifier><identifier>PMID: 36206339</identifier><language>eng</language><publisher>United States: American Association for the Advancement of Science</publisher><subject>Allergens ; Animals ; Biomedicine and Life Sciences ; Calcium - metabolism ; Calcium Channels - genetics ; Calcium Channels - metabolism ; Calcium Signaling ; Cytokines - metabolism ; E2F Transcription Factors ; Health and Medicine ; Inflammation ; Influenza A virus ; Mice ; ORAI1 Protein - genetics ; ORAI1 Protein - metabolism ; SciAdv r-articles ; Stromal Interaction Molecule 1 - metabolism ; Transcription Factors - metabolism ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Science advances, 2022-10, Vol.8 (40), p.eabn6552-eabn6552</ispartof><rights>Copyright © 2022 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC). 2022 The Authors</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-10f0e953df20fe0c595a152af719d13897bd97427cc8cb2d3b1ff8c83a67e4113</citedby><cites>FETCH-LOGICAL-c390t-10f0e953df20fe0c595a152af719d13897bd97427cc8cb2d3b1ff8c83a67e4113</cites><orcidid>0000-0002-1470-6421 ; 0000-0002-3510-3777 ; 0000-0001-7955-0256 ; 0000-0003-0978-2769 ; 0000-0001-8813-1061 ; 0000-0001-8974-7052 ; 0000-0003-3192-0865 ; 0000-0002-8090-4549 ; 0000-0002-5542-2994 ; 0000-0003-4317-5794 ; 0000-0003-1064-3010 ; 0000-0002-3637-8852 ; 0000-0002-1369-684X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9544339/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9544339/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,2883,2884,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36206339$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yin-Hu</creatorcontrib><creatorcontrib>Noyer, Lucile</creatorcontrib><creatorcontrib>Kahlfuss, Sascha</creatorcontrib><creatorcontrib>Raphael, Dimitrius</creatorcontrib><creatorcontrib>Tao, Anthony Y</creatorcontrib><creatorcontrib>Kaufmann, Ulrike</creatorcontrib><creatorcontrib>Zhu, Jingjie</creatorcontrib><creatorcontrib>Mitchell-Flack, Marisa</creatorcontrib><creatorcontrib>Sidhu, Ikjot</creatorcontrib><creatorcontrib>Zhou, Fang</creatorcontrib><creatorcontrib>Vaeth, Martin</creatorcontrib><creatorcontrib>Thomas, Paul G</creatorcontrib><creatorcontrib>Saunders, Sean P</creatorcontrib><creatorcontrib>Stauderman, Kenneth</creatorcontrib><creatorcontrib>Curotto de Lafaille, Maria A</creatorcontrib><creatorcontrib>Feske, Stefan</creatorcontrib><title>Distinct roles of ORAI1 in T cell-mediated allergic airway inflammation and immunity to influenza A virus infection</title><title>Science advances</title><addtitle>Sci Adv</addtitle><description>T cell activation and function depend on Ca
signals mediated by store-operated Ca
entry (SOCE) through Ca
release-activated Ca
(CRAC) channels formed by ORAI1 proteins. We here investigated how SOCE controls T cell function in pulmonary inflammation during a T helper 1 (T
1) cell-mediated response to influenza A virus (IAV) infection and T
2 cell-mediated allergic airway inflammation. T cell-specific deletion of
did not exacerbate pulmonary inflammation and viral burdens following IAV infection but protected mice from house dust mite-induced allergic airway inflammation. ORAI1 controlled the expression of genes including p53 and E2F transcription factors that regulate the cell cycle in T
2 cells in response to allergen stimulation and the expression of transcription factors and cytokines that regulate T
2 cell function. Systemic application of a CRAC channel blocker suppressed allergic airway inflammation without compromising immunity to IAV infection, suggesting that inhibition of SOCE is a potential treatment for allergic airway disease.</description><subject>Allergens</subject><subject>Animals</subject><subject>Biomedicine and Life Sciences</subject><subject>Calcium - metabolism</subject><subject>Calcium Channels - genetics</subject><subject>Calcium Channels - metabolism</subject><subject>Calcium Signaling</subject><subject>Cytokines - metabolism</subject><subject>E2F Transcription Factors</subject><subject>Health and Medicine</subject><subject>Inflammation</subject><subject>Influenza A virus</subject><subject>Mice</subject><subject>ORAI1 Protein - genetics</subject><subject>ORAI1 Protein - metabolism</subject><subject>SciAdv r-articles</subject><subject>Stromal Interaction Molecule 1 - metabolism</subject><subject>Transcription Factors - metabolism</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>2375-2548</issn><issn>2375-2548</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNpVkc1P4zAQxa0VqwWxve4R-cglxR9xEl-QKj4rISGh7tmaODYYJTbYTlH3r9-UFgSnseb9_Maeh9AfSuaUsuosaQfdeg6tr4RgP9AR47UomCibgy_nQzRL6ZkQQsuqElT-Qoe8YqTiXB6hdOlSdl5nHENvEg4W3z8slhQ7j1dYm74vBtM5yKbD0PcmPjqNwcU32EyI7WEYILvgMfgOu2EYvcsbnMO7OBr_D_ACr10c07Zj9Jb9jX5a6JOZ7esx-nt9tbq4Le7ub5YXi7tCc0lyQYklRgreWUasIVpIAVQwsDWVHeWNrNtO1iWrtW50yzreUmsb3XCoalNSyo_R-c73ZWynT2jjc4RevUQ3QNyoAE59V7x7Uo9hraQoy2k7k8Hp3iCG19GkrAaXtjsBb8KYFKsZp0I0rJzQ-Q7VMaQUjf0cQ4nahqV2Yal9WNOFk6-P-8Q_ouH_AZnllEw</recordid><startdate>20221007</startdate><enddate>20221007</enddate><creator>Wang, Yin-Hu</creator><creator>Noyer, Lucile</creator><creator>Kahlfuss, Sascha</creator><creator>Raphael, Dimitrius</creator><creator>Tao, Anthony Y</creator><creator>Kaufmann, Ulrike</creator><creator>Zhu, Jingjie</creator><creator>Mitchell-Flack, Marisa</creator><creator>Sidhu, Ikjot</creator><creator>Zhou, Fang</creator><creator>Vaeth, Martin</creator><creator>Thomas, Paul G</creator><creator>Saunders, Sean P</creator><creator>Stauderman, Kenneth</creator><creator>Curotto de Lafaille, Maria A</creator><creator>Feske, Stefan</creator><general>American Association for the Advancement of Science</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1470-6421</orcidid><orcidid>https://orcid.org/0000-0002-3510-3777</orcidid><orcidid>https://orcid.org/0000-0001-7955-0256</orcidid><orcidid>https://orcid.org/0000-0003-0978-2769</orcidid><orcidid>https://orcid.org/0000-0001-8813-1061</orcidid><orcidid>https://orcid.org/0000-0001-8974-7052</orcidid><orcidid>https://orcid.org/0000-0003-3192-0865</orcidid><orcidid>https://orcid.org/0000-0002-8090-4549</orcidid><orcidid>https://orcid.org/0000-0002-5542-2994</orcidid><orcidid>https://orcid.org/0000-0003-4317-5794</orcidid><orcidid>https://orcid.org/0000-0003-1064-3010</orcidid><orcidid>https://orcid.org/0000-0002-3637-8852</orcidid><orcidid>https://orcid.org/0000-0002-1369-684X</orcidid></search><sort><creationdate>20221007</creationdate><title>Distinct roles of ORAI1 in T cell-mediated allergic airway inflammation and immunity to influenza A virus infection</title><author>Wang, Yin-Hu ; Noyer, Lucile ; Kahlfuss, Sascha ; Raphael, Dimitrius ; Tao, Anthony Y ; Kaufmann, Ulrike ; Zhu, Jingjie ; Mitchell-Flack, Marisa ; Sidhu, Ikjot ; Zhou, Fang ; Vaeth, Martin ; Thomas, Paul G ; Saunders, Sean P ; Stauderman, Kenneth ; Curotto de Lafaille, Maria A ; Feske, Stefan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-10f0e953df20fe0c595a152af719d13897bd97427cc8cb2d3b1ff8c83a67e4113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Allergens</topic><topic>Animals</topic><topic>Biomedicine and Life Sciences</topic><topic>Calcium - metabolism</topic><topic>Calcium Channels - genetics</topic><topic>Calcium Channels - metabolism</topic><topic>Calcium Signaling</topic><topic>Cytokines - metabolism</topic><topic>E2F Transcription Factors</topic><topic>Health and Medicine</topic><topic>Inflammation</topic><topic>Influenza A virus</topic><topic>Mice</topic><topic>ORAI1 Protein - genetics</topic><topic>ORAI1 Protein - metabolism</topic><topic>SciAdv r-articles</topic><topic>Stromal Interaction Molecule 1 - metabolism</topic><topic>Transcription Factors - metabolism</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Yin-Hu</creatorcontrib><creatorcontrib>Noyer, Lucile</creatorcontrib><creatorcontrib>Kahlfuss, Sascha</creatorcontrib><creatorcontrib>Raphael, Dimitrius</creatorcontrib><creatorcontrib>Tao, Anthony Y</creatorcontrib><creatorcontrib>Kaufmann, Ulrike</creatorcontrib><creatorcontrib>Zhu, Jingjie</creatorcontrib><creatorcontrib>Mitchell-Flack, Marisa</creatorcontrib><creatorcontrib>Sidhu, Ikjot</creatorcontrib><creatorcontrib>Zhou, Fang</creatorcontrib><creatorcontrib>Vaeth, Martin</creatorcontrib><creatorcontrib>Thomas, Paul G</creatorcontrib><creatorcontrib>Saunders, Sean P</creatorcontrib><creatorcontrib>Stauderman, Kenneth</creatorcontrib><creatorcontrib>Curotto de Lafaille, Maria A</creatorcontrib><creatorcontrib>Feske, Stefan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Science advances</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Yin-Hu</au><au>Noyer, Lucile</au><au>Kahlfuss, Sascha</au><au>Raphael, Dimitrius</au><au>Tao, Anthony Y</au><au>Kaufmann, Ulrike</au><au>Zhu, Jingjie</au><au>Mitchell-Flack, Marisa</au><au>Sidhu, Ikjot</au><au>Zhou, Fang</au><au>Vaeth, Martin</au><au>Thomas, Paul G</au><au>Saunders, Sean P</au><au>Stauderman, Kenneth</au><au>Curotto de Lafaille, Maria A</au><au>Feske, Stefan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Distinct roles of ORAI1 in T cell-mediated allergic airway inflammation and immunity to influenza A virus infection</atitle><jtitle>Science advances</jtitle><addtitle>Sci Adv</addtitle><date>2022-10-07</date><risdate>2022</risdate><volume>8</volume><issue>40</issue><spage>eabn6552</spage><epage>eabn6552</epage><pages>eabn6552-eabn6552</pages><issn>2375-2548</issn><eissn>2375-2548</eissn><abstract>T cell activation and function depend on Ca
signals mediated by store-operated Ca
entry (SOCE) through Ca
release-activated Ca
(CRAC) channels formed by ORAI1 proteins. We here investigated how SOCE controls T cell function in pulmonary inflammation during a T helper 1 (T
1) cell-mediated response to influenza A virus (IAV) infection and T
2 cell-mediated allergic airway inflammation. T cell-specific deletion of
did not exacerbate pulmonary inflammation and viral burdens following IAV infection but protected mice from house dust mite-induced allergic airway inflammation. ORAI1 controlled the expression of genes including p53 and E2F transcription factors that regulate the cell cycle in T
2 cells in response to allergen stimulation and the expression of transcription factors and cytokines that regulate T
2 cell function. Systemic application of a CRAC channel blocker suppressed allergic airway inflammation without compromising immunity to IAV infection, suggesting that inhibition of SOCE is a potential treatment for allergic airway disease.</abstract><cop>United States</cop><pub>American Association for the Advancement of Science</pub><pmid>36206339</pmid><doi>10.1126/sciadv.abn6552</doi><orcidid>https://orcid.org/0000-0002-1470-6421</orcidid><orcidid>https://orcid.org/0000-0002-3510-3777</orcidid><orcidid>https://orcid.org/0000-0001-7955-0256</orcidid><orcidid>https://orcid.org/0000-0003-0978-2769</orcidid><orcidid>https://orcid.org/0000-0001-8813-1061</orcidid><orcidid>https://orcid.org/0000-0001-8974-7052</orcidid><orcidid>https://orcid.org/0000-0003-3192-0865</orcidid><orcidid>https://orcid.org/0000-0002-8090-4549</orcidid><orcidid>https://orcid.org/0000-0002-5542-2994</orcidid><orcidid>https://orcid.org/0000-0003-4317-5794</orcidid><orcidid>https://orcid.org/0000-0003-1064-3010</orcidid><orcidid>https://orcid.org/0000-0002-3637-8852</orcidid><orcidid>https://orcid.org/0000-0002-1369-684X</orcidid><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 2375-2548 |
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| source | Science Online_科学在线; PubMed Central |
| subjects | Allergens Animals Biomedicine and Life Sciences Calcium - metabolism Calcium Channels - genetics Calcium Channels - metabolism Calcium Signaling Cytokines - metabolism E2F Transcription Factors Health and Medicine Inflammation Influenza A virus Mice ORAI1 Protein - genetics ORAI1 Protein - metabolism SciAdv r-articles Stromal Interaction Molecule 1 - metabolism Transcription Factors - metabolism Tumor Suppressor Protein p53 - metabolism |
| title | Distinct roles of ORAI1 in T cell-mediated allergic airway inflammation and immunity to influenza A virus infection |
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