The deficiency of Gαq leads to enhanced T‐cell survival
We have previously reported that Gαq, the α subunit of the Gq protein, had important roles in dendritic cell migration, B‐cell survival and autoimmunity. In this study, we showed that the deficiency of Gαq led to enhanced T‐cell survival. Cultured Gnaq−/− T cells exhibited survival advantages both i...
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| Veröffentlicht in: | Immunology and cell biology 2014-10, Vol.92 (9), p.781-790 |
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| creator | Wang, Dashan Zhang, Yugao He, Yan Li, Yan Lund, Frances E Shi, Guixiu |
| description | We have previously reported that Gαq, the α subunit of the Gq protein, had important roles in dendritic cell migration, B‐cell survival and autoimmunity. In this study, we showed that the deficiency of Gαq led to enhanced T‐cell survival. Cultured Gnaq−/− T cells exhibited survival advantages both in medium alone and in the presence of anti‐CD3 stimulation. Gnaq−/− T cells still exhibited a survival advantage when they were cultured in the presence of interleukin (IL)‐2 or IL‐7. Gnaq−/− T cells were more resistant to activation‐induced cell death (AICD) in vitro. The survival advantage of Gnaq−/− T cells was further confirmed by transferring T cells into syngeneic hosts in vivo. Gαq deficiency might promote T‐cell survival by upregulated Bcl‐xL expression and downregulated Fas and FasL expressions. Furthermore, upon T‐cell receptor (TCR) ligation, Akt activity was increased in Gnaq−/− T cells in comparison with wild‐type (WT) T cells. The survival advantage of Gnaq−/− T cells was significantly attenuated after adding Akt inhibitor. Taken together, our data demonstrated a negative role of Gαq in regulating T‐cell survival. |
| doi_str_mv | 10.1038/icb.2014.53 |
| format | Article |
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In this study, we showed that the deficiency of Gαq led to enhanced T‐cell survival. Cultured Gnaq−/− T cells exhibited survival advantages both in medium alone and in the presence of anti‐CD3 stimulation. Gnaq−/− T cells still exhibited a survival advantage when they were cultured in the presence of interleukin (IL)‐2 or IL‐7. Gnaq−/− T cells were more resistant to activation‐induced cell death (AICD) in vitro. The survival advantage of Gnaq−/− T cells was further confirmed by transferring T cells into syngeneic hosts in vivo. Gαq deficiency might promote T‐cell survival by upregulated Bcl‐xL expression and downregulated Fas and FasL expressions. Furthermore, upon T‐cell receptor (TCR) ligation, Akt activity was increased in Gnaq−/− T cells in comparison with wild‐type (WT) T cells. The survival advantage of Gnaq−/− T cells was significantly attenuated after adding Akt inhibitor. Taken together, our data demonstrated a negative role of Gαq in regulating T‐cell survival.</description><identifier>ISSN: 0818-9641</identifier><identifier>EISSN: 1440-1711</identifier><identifier>DOI: 10.1038/icb.2014.53</identifier><identifier>PMID: 24957218</identifier><language>eng</language><publisher>United States: Nature Publishing Group</publisher><subject>Animals ; Cell Death - genetics ; Cell Death - immunology ; Cell Survival - genetics ; Cell Survival - immunology ; Down-Regulation - genetics ; Down-Regulation - immunology ; Fas Ligand Protein - genetics ; Fas Ligand Protein - immunology ; GTP-Binding Protein alpha Subunits, Gq-G11 - genetics ; GTP-Binding Protein alpha Subunits, Gq-G11 - immunology ; Interleukin-2 - genetics ; Interleukin-2 - immunology ; Interleukin-7 - genetics ; Interleukin-7 - immunology ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - immunology ; Receptors, Antigen, T-Cell - genetics ; Receptors, Antigen, T-Cell - immunology ; T-Lymphocytes - immunology ; Up-Regulation - genetics ; Up-Regulation - immunology</subject><ispartof>Immunology and cell biology, 2014-10, Vol.92 (9), p.781-790</ispartof><rights>2014 Australasian Society for Immunology Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3183-7e082631cc12553c805e4d7c8a3e6d4e60b5a45b5f33fb9b2ab601660c3b9d93</citedby><cites>FETCH-LOGICAL-c3183-7e082631cc12553c805e4d7c8a3e6d4e60b5a45b5f33fb9b2ab601660c3b9d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1038%2Ficb.2014.53$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1038%2Ficb.2014.53$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24957218$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Dashan</creatorcontrib><creatorcontrib>Zhang, Yugao</creatorcontrib><creatorcontrib>He, Yan</creatorcontrib><creatorcontrib>Li, Yan</creatorcontrib><creatorcontrib>Lund, Frances E</creatorcontrib><creatorcontrib>Shi, Guixiu</creatorcontrib><title>The deficiency of Gαq leads to enhanced T‐cell survival</title><title>Immunology and cell biology</title><addtitle>Immunol Cell Biol</addtitle><description>We have previously reported that Gαq, the α subunit of the Gq protein, had important roles in dendritic cell migration, B‐cell survival and autoimmunity. In this study, we showed that the deficiency of Gαq led to enhanced T‐cell survival. Cultured Gnaq−/− T cells exhibited survival advantages both in medium alone and in the presence of anti‐CD3 stimulation. Gnaq−/− T cells still exhibited a survival advantage when they were cultured in the presence of interleukin (IL)‐2 or IL‐7. Gnaq−/− T cells were more resistant to activation‐induced cell death (AICD) in vitro. The survival advantage of Gnaq−/− T cells was further confirmed by transferring T cells into syngeneic hosts in vivo. Gαq deficiency might promote T‐cell survival by upregulated Bcl‐xL expression and downregulated Fas and FasL expressions. Furthermore, upon T‐cell receptor (TCR) ligation, Akt activity was increased in Gnaq−/− T cells in comparison with wild‐type (WT) T cells. The survival advantage of Gnaq−/− T cells was significantly attenuated after adding Akt inhibitor. Taken together, our data demonstrated a negative role of Gαq in regulating T‐cell survival.</description><subject>Animals</subject><subject>Cell Death - genetics</subject><subject>Cell Death - immunology</subject><subject>Cell Survival - genetics</subject><subject>Cell Survival - immunology</subject><subject>Down-Regulation - genetics</subject><subject>Down-Regulation - immunology</subject><subject>Fas Ligand Protein - genetics</subject><subject>Fas Ligand Protein - immunology</subject><subject>GTP-Binding Protein alpha Subunits, Gq-G11 - genetics</subject><subject>GTP-Binding Protein alpha Subunits, Gq-G11 - immunology</subject><subject>Interleukin-2 - genetics</subject><subject>Interleukin-2 - immunology</subject><subject>Interleukin-7 - genetics</subject><subject>Interleukin-7 - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - immunology</subject><subject>Receptors, Antigen, T-Cell - genetics</subject><subject>Receptors, Antigen, T-Cell - immunology</subject><subject>T-Lymphocytes - immunology</subject><subject>Up-Regulation - genetics</subject><subject>Up-Regulation - immunology</subject><issn>0818-9641</issn><issn>1440-1711</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kDFOwzAUhi0EoqUwsaOMSCjFz44dhw0qKJVALNkt23lRg9KkjZuibhyBq3ARDsFJSNTCyPTe8OnTr4-Qc6BjoFxdF86OGYVoLPgBGUIU0RBigEMypApUmMgIBuTE-1dKacwUPyYDFiUiZqCG5CadY5BhXrgCK7cN6jyYfn2ughJN5oN1HWA1N5XDLEi_3z8clmXg22ZTbEx5So5yU3o8298RSR_u08lj-PQynU1un0LHQfEwRqqY5OAcMCG4U1RglMVOGY4yi1BSK0wkrMg5z21imbGSgpTUcZtkCR-Ry5122dSrFv1aLwrfDzEV1q3XIEEwEUuhOvRqh7qm9r7BXC-bYmGarQaq-1a6a6X7Vlrwjr7Yi1u7wOyP_Y3TAXwHvBUlbv9z6dnz5K7_O-0P20Jz6g</recordid><startdate>201410</startdate><enddate>201410</enddate><creator>Wang, Dashan</creator><creator>Zhang, Yugao</creator><creator>He, Yan</creator><creator>Li, Yan</creator><creator>Lund, Frances E</creator><creator>Shi, Guixiu</creator><general>Nature Publishing Group</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></search><sort><creationdate>201410</creationdate><title>The deficiency of Gαq leads to enhanced T‐cell survival</title><author>Wang, Dashan ; Zhang, Yugao ; He, Yan ; Li, Yan ; Lund, Frances E ; Shi, Guixiu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3183-7e082631cc12553c805e4d7c8a3e6d4e60b5a45b5f33fb9b2ab601660c3b9d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Cell Death - genetics</topic><topic>Cell Death - immunology</topic><topic>Cell Survival - genetics</topic><topic>Cell Survival - immunology</topic><topic>Down-Regulation - genetics</topic><topic>Down-Regulation - immunology</topic><topic>Fas Ligand Protein - genetics</topic><topic>Fas Ligand Protein - immunology</topic><topic>GTP-Binding Protein alpha Subunits, Gq-G11 - genetics</topic><topic>GTP-Binding Protein alpha Subunits, Gq-G11 - immunology</topic><topic>Interleukin-2 - genetics</topic><topic>Interleukin-2 - immunology</topic><topic>Interleukin-7 - genetics</topic><topic>Interleukin-7 - immunology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - immunology</topic><topic>Receptors, Antigen, T-Cell - genetics</topic><topic>Receptors, Antigen, T-Cell - immunology</topic><topic>T-Lymphocytes - immunology</topic><topic>Up-Regulation - genetics</topic><topic>Up-Regulation - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Dashan</creatorcontrib><creatorcontrib>Zhang, Yugao</creatorcontrib><creatorcontrib>He, Yan</creatorcontrib><creatorcontrib>Li, Yan</creatorcontrib><creatorcontrib>Lund, Frances E</creatorcontrib><creatorcontrib>Shi, Guixiu</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>Immunology and cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Dashan</au><au>Zhang, Yugao</au><au>He, Yan</au><au>Li, Yan</au><au>Lund, Frances E</au><au>Shi, Guixiu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The deficiency of Gαq leads to enhanced T‐cell survival</atitle><jtitle>Immunology and cell biology</jtitle><addtitle>Immunol Cell Biol</addtitle><date>2014-10</date><risdate>2014</risdate><volume>92</volume><issue>9</issue><spage>781</spage><epage>790</epage><pages>781-790</pages><issn>0818-9641</issn><eissn>1440-1711</eissn><abstract>We have previously reported that Gαq, the α subunit of the Gq protein, had important roles in dendritic cell migration, B‐cell survival and autoimmunity. In this study, we showed that the deficiency of Gαq led to enhanced T‐cell survival. Cultured Gnaq−/− T cells exhibited survival advantages both in medium alone and in the presence of anti‐CD3 stimulation. Gnaq−/− T cells still exhibited a survival advantage when they were cultured in the presence of interleukin (IL)‐2 or IL‐7. Gnaq−/− T cells were more resistant to activation‐induced cell death (AICD) in vitro. The survival advantage of Gnaq−/− T cells was further confirmed by transferring T cells into syngeneic hosts in vivo. Gαq deficiency might promote T‐cell survival by upregulated Bcl‐xL expression and downregulated Fas and FasL expressions. Furthermore, upon T‐cell receptor (TCR) ligation, Akt activity was increased in Gnaq−/− T cells in comparison with wild‐type (WT) T cells. The survival advantage of Gnaq−/− T cells was significantly attenuated after adding Akt inhibitor. Taken together, our data demonstrated a negative role of Gαq in regulating T‐cell survival.</abstract><cop>United States</cop><pub>Nature Publishing Group</pub><pmid>24957218</pmid><doi>10.1038/icb.2014.53</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals Cell Death - genetics Cell Death - immunology Cell Survival - genetics Cell Survival - immunology Down-Regulation - genetics Down-Regulation - immunology Fas Ligand Protein - genetics Fas Ligand Protein - immunology GTP-Binding Protein alpha Subunits, Gq-G11 - genetics GTP-Binding Protein alpha Subunits, Gq-G11 - immunology Interleukin-2 - genetics Interleukin-2 - immunology Interleukin-7 - genetics Interleukin-7 - immunology Mice Mice, Inbred C57BL Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - immunology Receptors, Antigen, T-Cell - genetics Receptors, Antigen, T-Cell - immunology T-Lymphocytes - immunology Up-Regulation - genetics Up-Regulation - immunology |
| title | The deficiency of Gαq leads to enhanced T‐cell survival |
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