Conditional deletion of Gata3 shows its essential function in TH1-TH2 responses
Expression of the transcription factor GATA-3 is strongly associated with T helper type 2 (T H 2) differentiation, but genetic evidence for its involvement in this process has been lacking. Here, we generated a conditional GATA-3-deficient mouse line. In vitro deletion of Gata3 diminished both inter...
Gespeichert in:
| Veröffentlicht in: | Nature immunology 2004-11, Vol.5 (11), p.1157-1165 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1165 |
|---|---|
| container_issue | 11 |
| container_start_page | 1157 |
| container_title | Nature immunology |
| container_volume | 5 |
| creator | Zhu, Jinfang Min, Booki Hu-Li, Jane Watson, Cynthia J Grinberg, Alex Wang, Qi Killeen, Nigel Urban, Joseph F Guo, Liying Paul, William E |
| description | Expression of the transcription factor GATA-3 is strongly associated with T helper type 2 (T
H
2) differentiation, but genetic evidence for its involvement in this process has been lacking. Here, we generated a conditional GATA-3-deficient mouse line.
In vitro
deletion of
Gata3
diminished both interleukin 4 (IL-4)–dependent and IL-4-independent T
H
2 cell differentiation; without GATA-3, T
H
1 differentiation occurred in the absence of IL-12 and interferon-γ.
Gata3
deletion limited the growth of T
H
2 cells but not T
H
1 cells. Deletion of
Gata3
from established T
H
2 cells abolished IL-5 and IL-13 but not IL-4 production.
In vivo
deletion of
Gata3
using OX40-Cre eliminated T
H
2 responses and allowed the development of interferon-γ-producing cells in mice infected with
Nippostrongylus brasiliensis
. Thus, GATA-3 serves as a principal switch in determining T
H
1-T
H
2 responses. |
| doi_str_mv | 10.1038/ni1128 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_journals_222751902</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A188812199</galeid><sourcerecordid>A188812199</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3628-c41d5d5aecbefe2642e2d50e2b0363718575a6ae33b6222a6a5e288465616f5b3</originalsourceid><addsrcrecordid>eNpt0VFLwzAQB_AiCs6pn6EoKD50JmmTpo9j6DYQBjqfQ9ZeZ0aXzFyH-u3NrCgTuYf8Cb87OC6KzikZUJLKW2soZfIg6lHOioQVVBz-ZCKPoxPEFSE0y0XWi2YjZyvTGmd1E1fQwC7Gro7HutVpjC_uDWPTYgyIYFsTVL215ZcyNp5PaDKfsNgDbpxFwNPoqNYNwtn324-e7-_mo0nyMBtPR8OHpEwFk0mZ0YpXXEO5gBqYyBiwihNgC5KKNKeS51wLDWm6EIyxEDkwKTPBBRU1X6T96KKbu_HudQvYqpXb-rAEquBzTgvCArrs0FI3oIytXet1uTZYqiGVUlJGiyKowT8qVAVrUzoLtQn_ew03ew3BtPDeLvUWUU2fHvftVWdL7xA91GrjzVr7D0WJ2p1LdecK8LqDGIBdgv9d6I_8BGI_kFs</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>222751902</pqid></control><display><type>article</type><title>Conditional deletion of Gata3 shows its essential function in TH1-TH2 responses</title><source>SpringerLink Journals</source><source>Nature Journals Online</source><creator>Zhu, Jinfang ; Min, Booki ; Hu-Li, Jane ; Watson, Cynthia J ; Grinberg, Alex ; Wang, Qi ; Killeen, Nigel ; Urban, Joseph F ; Guo, Liying ; Paul, William E</creator><creatorcontrib>Zhu, Jinfang ; Min, Booki ; Hu-Li, Jane ; Watson, Cynthia J ; Grinberg, Alex ; Wang, Qi ; Killeen, Nigel ; Urban, Joseph F ; Guo, Liying ; Paul, William E</creatorcontrib><description>Expression of the transcription factor GATA-3 is strongly associated with T helper type 2 (T
H
2) differentiation, but genetic evidence for its involvement in this process has been lacking. Here, we generated a conditional GATA-3-deficient mouse line.
In vitro
deletion of
Gata3
diminished both interleukin 4 (IL-4)–dependent and IL-4-independent T
H
2 cell differentiation; without GATA-3, T
H
1 differentiation occurred in the absence of IL-12 and interferon-γ.
Gata3
deletion limited the growth of T
H
2 cells but not T
H
1 cells. Deletion of
Gata3
from established T
H
2 cells abolished IL-5 and IL-13 but not IL-4 production.
In vivo
deletion of
Gata3
using OX40-Cre eliminated T
H
2 responses and allowed the development of interferon-γ-producing cells in mice infected with
Nippostrongylus brasiliensis
. Thus, GATA-3 serves as a principal switch in determining T
H
1-T
H
2 responses.</description><identifier>ISSN: 1529-2908</identifier><identifier>EISSN: 1529-2916</identifier><identifier>DOI: 10.1038/ni1128</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Biomedical and Life Sciences ; Biomedicine ; Cell differentiation ; Immunology ; Infectious Diseases</subject><ispartof>Nature immunology, 2004-11, Vol.5 (11), p.1157-1165</ispartof><rights>Springer Nature America, Inc. 2004</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Nov 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3628-c41d5d5aecbefe2642e2d50e2b0363718575a6ae33b6222a6a5e288465616f5b3</citedby><cites>FETCH-LOGICAL-c3628-c41d5d5aecbefe2642e2d50e2b0363718575a6ae33b6222a6a5e288465616f5b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ni1128$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ni1128$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids></links><search><creatorcontrib>Zhu, Jinfang</creatorcontrib><creatorcontrib>Min, Booki</creatorcontrib><creatorcontrib>Hu-Li, Jane</creatorcontrib><creatorcontrib>Watson, Cynthia J</creatorcontrib><creatorcontrib>Grinberg, Alex</creatorcontrib><creatorcontrib>Wang, Qi</creatorcontrib><creatorcontrib>Killeen, Nigel</creatorcontrib><creatorcontrib>Urban, Joseph F</creatorcontrib><creatorcontrib>Guo, Liying</creatorcontrib><creatorcontrib>Paul, William E</creatorcontrib><title>Conditional deletion of Gata3 shows its essential function in TH1-TH2 responses</title><title>Nature immunology</title><addtitle>Nat Immunol</addtitle><description>Expression of the transcription factor GATA-3 is strongly associated with T helper type 2 (T
H
2) differentiation, but genetic evidence for its involvement in this process has been lacking. Here, we generated a conditional GATA-3-deficient mouse line.
In vitro
deletion of
Gata3
diminished both interleukin 4 (IL-4)–dependent and IL-4-independent T
H
2 cell differentiation; without GATA-3, T
H
1 differentiation occurred in the absence of IL-12 and interferon-γ.
Gata3
deletion limited the growth of T
H
2 cells but not T
H
1 cells. Deletion of
Gata3
from established T
H
2 cells abolished IL-5 and IL-13 but not IL-4 production.
In vivo
deletion of
Gata3
using OX40-Cre eliminated T
H
2 responses and allowed the development of interferon-γ-producing cells in mice infected with
Nippostrongylus brasiliensis
. Thus, GATA-3 serves as a principal switch in determining T
H
1-T
H
2 responses.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell differentiation</subject><subject>Immunology</subject><subject>Infectious Diseases</subject><issn>1529-2908</issn><issn>1529-2916</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpt0VFLwzAQB_AiCs6pn6EoKD50JmmTpo9j6DYQBjqfQ9ZeZ0aXzFyH-u3NrCgTuYf8Cb87OC6KzikZUJLKW2soZfIg6lHOioQVVBz-ZCKPoxPEFSE0y0XWi2YjZyvTGmd1E1fQwC7Gro7HutVpjC_uDWPTYgyIYFsTVL215ZcyNp5PaDKfsNgDbpxFwNPoqNYNwtn324-e7-_mo0nyMBtPR8OHpEwFk0mZ0YpXXEO5gBqYyBiwihNgC5KKNKeS51wLDWm6EIyxEDkwKTPBBRU1X6T96KKbu_HudQvYqpXb-rAEquBzTgvCArrs0FI3oIytXet1uTZYqiGVUlJGiyKowT8qVAVrUzoLtQn_ew03ew3BtPDeLvUWUU2fHvftVWdL7xA91GrjzVr7D0WJ2p1LdecK8LqDGIBdgv9d6I_8BGI_kFs</recordid><startdate>20041101</startdate><enddate>20041101</enddate><creator>Zhu, Jinfang</creator><creator>Min, Booki</creator><creator>Hu-Li, Jane</creator><creator>Watson, Cynthia J</creator><creator>Grinberg, Alex</creator><creator>Wang, Qi</creator><creator>Killeen, Nigel</creator><creator>Urban, Joseph F</creator><creator>Guo, Liying</creator><creator>Paul, William E</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>AAYXX</scope><scope>CITATION</scope><scope>ISR</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope></search><sort><creationdate>20041101</creationdate><title>Conditional deletion of Gata3 shows its essential function in TH1-TH2 responses</title><author>Zhu, Jinfang ; Min, Booki ; Hu-Li, Jane ; Watson, Cynthia J ; Grinberg, Alex ; Wang, Qi ; Killeen, Nigel ; Urban, Joseph F ; Guo, Liying ; Paul, William E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3628-c41d5d5aecbefe2642e2d50e2b0363718575a6ae33b6222a6a5e288465616f5b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell differentiation</topic><topic>Immunology</topic><topic>Infectious Diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Jinfang</creatorcontrib><creatorcontrib>Min, Booki</creatorcontrib><creatorcontrib>Hu-Li, Jane</creatorcontrib><creatorcontrib>Watson, Cynthia J</creatorcontrib><creatorcontrib>Grinberg, Alex</creatorcontrib><creatorcontrib>Wang, Qi</creatorcontrib><creatorcontrib>Killeen, Nigel</creatorcontrib><creatorcontrib>Urban, Joseph F</creatorcontrib><creatorcontrib>Guo, Liying</creatorcontrib><creatorcontrib>Paul, William E</creatorcontrib><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</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 One Sustainability</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>Engineering Research Database</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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><jtitle>Nature immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Jinfang</au><au>Min, Booki</au><au>Hu-Li, Jane</au><au>Watson, Cynthia J</au><au>Grinberg, Alex</au><au>Wang, Qi</au><au>Killeen, Nigel</au><au>Urban, Joseph F</au><au>Guo, Liying</au><au>Paul, William E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Conditional deletion of Gata3 shows its essential function in TH1-TH2 responses</atitle><jtitle>Nature immunology</jtitle><stitle>Nat Immunol</stitle><date>2004-11-01</date><risdate>2004</risdate><volume>5</volume><issue>11</issue><spage>1157</spage><epage>1165</epage><pages>1157-1165</pages><issn>1529-2908</issn><eissn>1529-2916</eissn><abstract>Expression of the transcription factor GATA-3 is strongly associated with T helper type 2 (T
H
2) differentiation, but genetic evidence for its involvement in this process has been lacking. Here, we generated a conditional GATA-3-deficient mouse line.
In vitro
deletion of
Gata3
diminished both interleukin 4 (IL-4)–dependent and IL-4-independent T
H
2 cell differentiation; without GATA-3, T
H
1 differentiation occurred in the absence of IL-12 and interferon-γ.
Gata3
deletion limited the growth of T
H
2 cells but not T
H
1 cells. Deletion of
Gata3
from established T
H
2 cells abolished IL-5 and IL-13 but not IL-4 production.
In vivo
deletion of
Gata3
using OX40-Cre eliminated T
H
2 responses and allowed the development of interferon-γ-producing cells in mice infected with
Nippostrongylus brasiliensis
. Thus, GATA-3 serves as a principal switch in determining T
H
1-T
H
2 responses.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><doi>10.1038/ni1128</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1529-2908 |
| ispartof | Nature immunology, 2004-11, Vol.5 (11), p.1157-1165 |
| issn | 1529-2908 1529-2916 |
| language | eng |
| recordid | cdi_proquest_journals_222751902 |
| source | SpringerLink Journals; Nature Journals Online |
| subjects | Biomedical and Life Sciences Biomedicine Cell differentiation Immunology Infectious Diseases |
| title | Conditional deletion of Gata3 shows its essential function in TH1-TH2 responses |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T20%3A32%3A11IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Conditional%20deletion%20of%20Gata3%20shows%20its%20essential%20function%20in%20TH1-TH2%20responses&rft.jtitle=Nature%20immunology&rft.au=Zhu,%20Jinfang&rft.date=2004-11-01&rft.volume=5&rft.issue=11&rft.spage=1157&rft.epage=1165&rft.pages=1157-1165&rft.issn=1529-2908&rft.eissn=1529-2916&rft_id=info:doi/10.1038/ni1128&rft_dat=%3Cgale_proqu%3EA188812199%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=222751902&rft_id=info:pmid/&rft_galeid=A188812199&rfr_iscdi=true |