Survivin facilitates T‐helper 2–biased inflammation in the airway
Background The biased T helper 2 (Th2) responses play a critical role in the pathogenesis of allergy. The underlying mechanism is not fully understood yet. Survivin can regulate multiple cellular activities. This study aims to elucidate the role of survivin in the development and maintenance of Th2...
Gespeichert in:
| Veröffentlicht in: | International forum of allergy & rhinology 2019-06, Vol.9 (6), p.656-664 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 664 |
|---|---|
| container_issue | 6 |
| container_start_page | 656 |
| container_title | International forum of allergy & rhinology |
| container_volume | 9 |
| creator | Xue, Jin‐Mei Zhao, Mei‐Zhen Ma, Fei Li, Shan‐Shan Mo, Li‐Hua Zeng, Xian‐Hai Wu, Yong‐Jin Liu, Jiang‐Qi Hu, Tian‐Yong Xie, Rui‐Di Liu, Zhi‐Gang Zhao, Chang‐Qing Yang, Ping‐Chang |
| description | Background
The biased T helper 2 (Th2) responses play a critical role in the pathogenesis of allergy. The underlying mechanism is not fully understood yet. Survivin can regulate multiple cellular activities. This study aims to elucidate the role of survivin in the development and maintenance of Th2 polarization.
Methods
CD4+ T cells were isolated from blood samples collected from patients with allergic asthma (AS) and HS control (HS) subjects. Mice carrying CD4+ T cells with survivin knockout (KO mice) were employed to test the role of survivin in the development of the biased Th2 responses.
Results
KO mice failed to induce airway allergy. Peripheral CD4+ T cells expressed survivin, which was higher in the AS group than that in the HS group. Naive CD4+ T cells with higher expression of survivin were prone to differentiating into Th2 cells. Survivin bound to the Il4 promoter in CD4+ T cells to enhance Il4 gene transcription. The expression of Fas was lower in CD4+ T cells of the AS group than that in the HS group. Overexpression of survivin suppressed the expression of Fas and impaired the activation‐induced cell death (AICD) of CD4+ T cells.
Conclusion
Survivin facilitates the development of biased Th2 polarization through promoting expression of interleukin 4 (IL‐4) and impairing the AICD machinery of CD4+ T cells. To modulate the expression of survivin in CD4+ T cells has the translational potential in the treatment of allergic diseases. |
| doi_str_mv | 10.1002/alr.22301 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2179484108</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2179484108</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3251-b2ba0aeb5002dc4fc8dbd2d402a842f91dd5d6e59a6f43288332f037ff995d373</originalsourceid><addsrcrecordid>eNp1kMtKAzEUQIMottQu_AGZpS6mzXMey1LqAwYEreuQmSQ0kpmpyUxLd_0EwT_slzg6tTuzublwOFwOANcIThCEeCqsm2BMIDoDQwwpDqM0oeenfxwNwNj7d9g9hhhD8SUYEBgjFqfRECxeW7cxG1MFWhTGmkY0ygfLw_5zpexauQAf9l-5EV7JwFTairIUjamrbgmalQqEcVuxuwIXWlivxsc5Am_3i-X8McyeH57msywsCGYozHEuoFA56-6WBdVFInOJJYVYJBTrFEnJZKRYKiJNCU4SQrCGJNY6TZkkMRmB2967dvVHq3zDS-MLZa2oVN16jlGc0oQimHToXY8WrvbeKc3XzpTC7TiC_Ccc78Lx33Ade3PUtnmp5In8y9QB0x7YGqt2_5v4LHvpld_VzXhy</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2179484108</pqid></control><display><type>article</type><title>Survivin facilitates T‐helper 2–biased inflammation in the airway</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Xue, Jin‐Mei ; Zhao, Mei‐Zhen ; Ma, Fei ; Li, Shan‐Shan ; Mo, Li‐Hua ; Zeng, Xian‐Hai ; Wu, Yong‐Jin ; Liu, Jiang‐Qi ; Hu, Tian‐Yong ; Xie, Rui‐Di ; Liu, Zhi‐Gang ; Zhao, Chang‐Qing ; Yang, Ping‐Chang</creator><creatorcontrib>Xue, Jin‐Mei ; Zhao, Mei‐Zhen ; Ma, Fei ; Li, Shan‐Shan ; Mo, Li‐Hua ; Zeng, Xian‐Hai ; Wu, Yong‐Jin ; Liu, Jiang‐Qi ; Hu, Tian‐Yong ; Xie, Rui‐Di ; Liu, Zhi‐Gang ; Zhao, Chang‐Qing ; Yang, Ping‐Chang</creatorcontrib><description>Background
The biased T helper 2 (Th2) responses play a critical role in the pathogenesis of allergy. The underlying mechanism is not fully understood yet. Survivin can regulate multiple cellular activities. This study aims to elucidate the role of survivin in the development and maintenance of Th2 polarization.
Methods
CD4+ T cells were isolated from blood samples collected from patients with allergic asthma (AS) and HS control (HS) subjects. Mice carrying CD4+ T cells with survivin knockout (KO mice) were employed to test the role of survivin in the development of the biased Th2 responses.
Results
KO mice failed to induce airway allergy. Peripheral CD4+ T cells expressed survivin, which was higher in the AS group than that in the HS group. Naive CD4+ T cells with higher expression of survivin were prone to differentiating into Th2 cells. Survivin bound to the Il4 promoter in CD4+ T cells to enhance Il4 gene transcription. The expression of Fas was lower in CD4+ T cells of the AS group than that in the HS group. Overexpression of survivin suppressed the expression of Fas and impaired the activation‐induced cell death (AICD) of CD4+ T cells.
Conclusion
Survivin facilitates the development of biased Th2 polarization through promoting expression of interleukin 4 (IL‐4) and impairing the AICD machinery of CD4+ T cells. To modulate the expression of survivin in CD4+ T cells has the translational potential in the treatment of allergic diseases.</description><identifier>ISSN: 2042-6976</identifier><identifier>EISSN: 2042-6984</identifier><identifier>DOI: 10.1002/alr.22301</identifier><identifier>PMID: 30715796</identifier><language>eng</language><publisher>United States</publisher><subject>Adult ; allergy ; Animals ; apoptosis ; Asthma - immunology ; Asthma - pathology ; CD4 T cell ; Cell Death ; Female ; Gene Expression ; Humans ; Inflammation ; Interleukin-4 - genetics ; Male ; Mice ; Mice, Knockout ; survivin ; Survivin - deficiency ; Survivin - genetics ; Survivin - metabolism ; T-Lymphocytes - immunology ; T-Lymphocytes - metabolism ; T-Lymphocytes - pathology ; Th2 Cells - immunology ; Th2 response</subject><ispartof>International forum of allergy & rhinology, 2019-06, Vol.9 (6), p.656-664</ispartof><rights>2019 ARS‐AAOA, LLC</rights><rights>2019 ARS-AAOA, LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3251-b2ba0aeb5002dc4fc8dbd2d402a842f91dd5d6e59a6f43288332f037ff995d373</citedby><cites>FETCH-LOGICAL-c3251-b2ba0aeb5002dc4fc8dbd2d402a842f91dd5d6e59a6f43288332f037ff995d373</cites><orcidid>0000-0002-3650-0416 ; 0000-0001-6627-5726</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%2Falr.22301$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Falr.22301$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30715796$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xue, Jin‐Mei</creatorcontrib><creatorcontrib>Zhao, Mei‐Zhen</creatorcontrib><creatorcontrib>Ma, Fei</creatorcontrib><creatorcontrib>Li, Shan‐Shan</creatorcontrib><creatorcontrib>Mo, Li‐Hua</creatorcontrib><creatorcontrib>Zeng, Xian‐Hai</creatorcontrib><creatorcontrib>Wu, Yong‐Jin</creatorcontrib><creatorcontrib>Liu, Jiang‐Qi</creatorcontrib><creatorcontrib>Hu, Tian‐Yong</creatorcontrib><creatorcontrib>Xie, Rui‐Di</creatorcontrib><creatorcontrib>Liu, Zhi‐Gang</creatorcontrib><creatorcontrib>Zhao, Chang‐Qing</creatorcontrib><creatorcontrib>Yang, Ping‐Chang</creatorcontrib><title>Survivin facilitates T‐helper 2–biased inflammation in the airway</title><title>International forum of allergy & rhinology</title><addtitle>Int Forum Allergy Rhinol</addtitle><description>Background
The biased T helper 2 (Th2) responses play a critical role in the pathogenesis of allergy. The underlying mechanism is not fully understood yet. Survivin can regulate multiple cellular activities. This study aims to elucidate the role of survivin in the development and maintenance of Th2 polarization.
Methods
CD4+ T cells were isolated from blood samples collected from patients with allergic asthma (AS) and HS control (HS) subjects. Mice carrying CD4+ T cells with survivin knockout (KO mice) were employed to test the role of survivin in the development of the biased Th2 responses.
Results
KO mice failed to induce airway allergy. Peripheral CD4+ T cells expressed survivin, which was higher in the AS group than that in the HS group. Naive CD4+ T cells with higher expression of survivin were prone to differentiating into Th2 cells. Survivin bound to the Il4 promoter in CD4+ T cells to enhance Il4 gene transcription. The expression of Fas was lower in CD4+ T cells of the AS group than that in the HS group. Overexpression of survivin suppressed the expression of Fas and impaired the activation‐induced cell death (AICD) of CD4+ T cells.
Conclusion
Survivin facilitates the development of biased Th2 polarization through promoting expression of interleukin 4 (IL‐4) and impairing the AICD machinery of CD4+ T cells. To modulate the expression of survivin in CD4+ T cells has the translational potential in the treatment of allergic diseases.</description><subject>Adult</subject><subject>allergy</subject><subject>Animals</subject><subject>apoptosis</subject><subject>Asthma - immunology</subject><subject>Asthma - pathology</subject><subject>CD4 T cell</subject><subject>Cell Death</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Interleukin-4 - genetics</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>survivin</subject><subject>Survivin - deficiency</subject><subject>Survivin - genetics</subject><subject>Survivin - metabolism</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - metabolism</subject><subject>T-Lymphocytes - pathology</subject><subject>Th2 Cells - immunology</subject><subject>Th2 response</subject><issn>2042-6976</issn><issn>2042-6984</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtKAzEUQIMottQu_AGZpS6mzXMey1LqAwYEreuQmSQ0kpmpyUxLd_0EwT_slzg6tTuzublwOFwOANcIThCEeCqsm2BMIDoDQwwpDqM0oeenfxwNwNj7d9g9hhhD8SUYEBgjFqfRECxeW7cxG1MFWhTGmkY0ygfLw_5zpexauQAf9l-5EV7JwFTairIUjamrbgmalQqEcVuxuwIXWlivxsc5Am_3i-X8McyeH57msywsCGYozHEuoFA56-6WBdVFInOJJYVYJBTrFEnJZKRYKiJNCU4SQrCGJNY6TZkkMRmB2967dvVHq3zDS-MLZa2oVN16jlGc0oQimHToXY8WrvbeKc3XzpTC7TiC_Ccc78Lx33Ade3PUtnmp5In8y9QB0x7YGqt2_5v4LHvpld_VzXhy</recordid><startdate>201906</startdate><enddate>201906</enddate><creator>Xue, Jin‐Mei</creator><creator>Zhao, Mei‐Zhen</creator><creator>Ma, Fei</creator><creator>Li, Shan‐Shan</creator><creator>Mo, Li‐Hua</creator><creator>Zeng, Xian‐Hai</creator><creator>Wu, Yong‐Jin</creator><creator>Liu, Jiang‐Qi</creator><creator>Hu, Tian‐Yong</creator><creator>Xie, Rui‐Di</creator><creator>Liu, Zhi‐Gang</creator><creator>Zhao, Chang‐Qing</creator><creator>Yang, Ping‐Chang</creator><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><orcidid>https://orcid.org/0000-0002-3650-0416</orcidid><orcidid>https://orcid.org/0000-0001-6627-5726</orcidid></search><sort><creationdate>201906</creationdate><title>Survivin facilitates T‐helper 2–biased inflammation in the airway</title><author>Xue, Jin‐Mei ; Zhao, Mei‐Zhen ; Ma, Fei ; Li, Shan‐Shan ; Mo, Li‐Hua ; Zeng, Xian‐Hai ; Wu, Yong‐Jin ; Liu, Jiang‐Qi ; Hu, Tian‐Yong ; Xie, Rui‐Di ; Liu, Zhi‐Gang ; Zhao, Chang‐Qing ; Yang, Ping‐Chang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3251-b2ba0aeb5002dc4fc8dbd2d402a842f91dd5d6e59a6f43288332f037ff995d373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adult</topic><topic>allergy</topic><topic>Animals</topic><topic>apoptosis</topic><topic>Asthma - immunology</topic><topic>Asthma - pathology</topic><topic>CD4 T cell</topic><topic>Cell Death</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Interleukin-4 - genetics</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>survivin</topic><topic>Survivin - deficiency</topic><topic>Survivin - genetics</topic><topic>Survivin - metabolism</topic><topic>T-Lymphocytes - immunology</topic><topic>T-Lymphocytes - metabolism</topic><topic>T-Lymphocytes - pathology</topic><topic>Th2 Cells - immunology</topic><topic>Th2 response</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xue, Jin‐Mei</creatorcontrib><creatorcontrib>Zhao, Mei‐Zhen</creatorcontrib><creatorcontrib>Ma, Fei</creatorcontrib><creatorcontrib>Li, Shan‐Shan</creatorcontrib><creatorcontrib>Mo, Li‐Hua</creatorcontrib><creatorcontrib>Zeng, Xian‐Hai</creatorcontrib><creatorcontrib>Wu, Yong‐Jin</creatorcontrib><creatorcontrib>Liu, Jiang‐Qi</creatorcontrib><creatorcontrib>Hu, Tian‐Yong</creatorcontrib><creatorcontrib>Xie, Rui‐Di</creatorcontrib><creatorcontrib>Liu, Zhi‐Gang</creatorcontrib><creatorcontrib>Zhao, Chang‐Qing</creatorcontrib><creatorcontrib>Yang, Ping‐Chang</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><jtitle>International forum of allergy & rhinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xue, Jin‐Mei</au><au>Zhao, Mei‐Zhen</au><au>Ma, Fei</au><au>Li, Shan‐Shan</au><au>Mo, Li‐Hua</au><au>Zeng, Xian‐Hai</au><au>Wu, Yong‐Jin</au><au>Liu, Jiang‐Qi</au><au>Hu, Tian‐Yong</au><au>Xie, Rui‐Di</au><au>Liu, Zhi‐Gang</au><au>Zhao, Chang‐Qing</au><au>Yang, Ping‐Chang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Survivin facilitates T‐helper 2–biased inflammation in the airway</atitle><jtitle>International forum of allergy & rhinology</jtitle><addtitle>Int Forum Allergy Rhinol</addtitle><date>2019-06</date><risdate>2019</risdate><volume>9</volume><issue>6</issue><spage>656</spage><epage>664</epage><pages>656-664</pages><issn>2042-6976</issn><eissn>2042-6984</eissn><abstract>Background
The biased T helper 2 (Th2) responses play a critical role in the pathogenesis of allergy. The underlying mechanism is not fully understood yet. Survivin can regulate multiple cellular activities. This study aims to elucidate the role of survivin in the development and maintenance of Th2 polarization.
Methods
CD4+ T cells were isolated from blood samples collected from patients with allergic asthma (AS) and HS control (HS) subjects. Mice carrying CD4+ T cells with survivin knockout (KO mice) were employed to test the role of survivin in the development of the biased Th2 responses.
Results
KO mice failed to induce airway allergy. Peripheral CD4+ T cells expressed survivin, which was higher in the AS group than that in the HS group. Naive CD4+ T cells with higher expression of survivin were prone to differentiating into Th2 cells. Survivin bound to the Il4 promoter in CD4+ T cells to enhance Il4 gene transcription. The expression of Fas was lower in CD4+ T cells of the AS group than that in the HS group. Overexpression of survivin suppressed the expression of Fas and impaired the activation‐induced cell death (AICD) of CD4+ T cells.
Conclusion
Survivin facilitates the development of biased Th2 polarization through promoting expression of interleukin 4 (IL‐4) and impairing the AICD machinery of CD4+ T cells. To modulate the expression of survivin in CD4+ T cells has the translational potential in the treatment of allergic diseases.</abstract><cop>United States</cop><pmid>30715796</pmid><doi>10.1002/alr.22301</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-3650-0416</orcidid><orcidid>https://orcid.org/0000-0001-6627-5726</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2042-6976 |
| ispartof | International forum of allergy & rhinology, 2019-06, Vol.9 (6), p.656-664 |
| issn | 2042-6976 2042-6984 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2179484108 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Adult allergy Animals apoptosis Asthma - immunology Asthma - pathology CD4 T cell Cell Death Female Gene Expression Humans Inflammation Interleukin-4 - genetics Male Mice Mice, Knockout survivin Survivin - deficiency Survivin - genetics Survivin - metabolism T-Lymphocytes - immunology T-Lymphocytes - metabolism T-Lymphocytes - pathology Th2 Cells - immunology Th2 response |
| title | Survivin facilitates T‐helper 2–biased inflammation in the airway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T03%3A42%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Survivin%20facilitates%20T%E2%80%90helper%202%E2%80%93biased%20inflammation%20in%20the%20airway&rft.jtitle=International%20forum%20of%20allergy%20&%20rhinology&rft.au=Xue,%20Jin%E2%80%90Mei&rft.date=2019-06&rft.volume=9&rft.issue=6&rft.spage=656&rft.epage=664&rft.pages=656-664&rft.issn=2042-6976&rft.eissn=2042-6984&rft_id=info:doi/10.1002/alr.22301&rft_dat=%3Cproquest_cross%3E2179484108%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2179484108&rft_id=info:pmid/30715796&rfr_iscdi=true |