Defective survival of naive CD8 + T lymphocytes in the absence of the β3 regulatory subunit of voltage-gated calcium channels
T cell activation triggers large calcium fluxes. Flavell and colleagues show tonic calcium signaling via Ca v 1.4-β3 channels are needed for the survival and homeostasis of naive CD8 + T cells. The survival of T lymphocytes requires sustained, Ca 2+ influx–dependent gene expression. The molecular me...
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| Veröffentlicht in: | Nature immunology 2009, Vol.10 (12), p.1275-1282 |
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| container_title | Nature immunology |
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| creator | Badou, Abdallah Flockerzi, Veit McRory, John E Flavell, Richard A Jha, Mithilesh K Meissner, Marcel Freichel, Marc |
| description | T cell activation triggers large calcium fluxes. Flavell and colleagues show tonic calcium signaling via Ca
v
1.4-β3 channels are needed for the survival and homeostasis of naive CD8
+
T cells.
The survival of T lymphocytes requires sustained, Ca
2+
influx–dependent gene expression. The molecular mechanism that governs sustained Ca
2+
influx in naive T lymphocytes is unknown. Here we report an essential role for the β3 regulatory subunit of voltage-gated calcium (Ca
v
) channels in the maintenance of naive CD8
+
T cells. Deficiency in β3 resulted in a profound survival defect of CD8
+
T cells. This defect correlated with depletion of the pore-forming subunit Ca
v
1.4 and attenuation of T cell antigen receptor (TCR)-mediated global Ca
2+
entry in CD8
+
T cells. Ca
v
1.4 and β3 associated with T cell signaling machinery and Ca
v
1.4 localized in lipid rafts. Our data demonstrate a mechanism by which Ca
2+
entry is controlled by a Ca
v
1.4-β3 channel complex in T cells. |
| doi_str_mv | 10.1038/ni.1793 |
| format | Article |
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v
1.4-β3 channels are needed for the survival and homeostasis of naive CD8
+
T cells.
The survival of T lymphocytes requires sustained, Ca
2+
influx–dependent gene expression. The molecular mechanism that governs sustained Ca
2+
influx in naive T lymphocytes is unknown. Here we report an essential role for the β3 regulatory subunit of voltage-gated calcium (Ca
v
) channels in the maintenance of naive CD8
+
T cells. Deficiency in β3 resulted in a profound survival defect of CD8
+
T cells. This defect correlated with depletion of the pore-forming subunit Ca
v
1.4 and attenuation of T cell antigen receptor (TCR)-mediated global Ca
2+
entry in CD8
+
T cells. Ca
v
1.4 and β3 associated with T cell signaling machinery and Ca
v
1.4 localized in lipid rafts. Our data demonstrate a mechanism by which Ca
2+
entry is controlled by a Ca
v
1.4-β3 channel complex in T cells.</description><identifier>ISSN: 1529-2908</identifier><identifier>EISSN: 1529-2916</identifier><identifier>DOI: 10.1038/ni.1793</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Biomedical and Life Sciences ; Biomedicine ; Immunology ; Infectious Diseases</subject><ispartof>Nature immunology, 2009, Vol.10 (12), p.1275-1282</ispartof><rights>Springer Nature America, Inc. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2283-c8079b1bdb4dc3ae912b13fa4450c7a4e5bcad028bd152699910d662058eecd93</citedby><cites>FETCH-LOGICAL-c2283-c8079b1bdb4dc3ae912b13fa4450c7a4e5bcad028bd152699910d662058eecd93</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/ni.1793$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ni.1793$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27907,27908,41471,42540,51302</link.rule.ids></links><search><creatorcontrib>Badou, Abdallah</creatorcontrib><creatorcontrib>Flockerzi, Veit</creatorcontrib><creatorcontrib>McRory, John E</creatorcontrib><creatorcontrib>Flavell, Richard A</creatorcontrib><creatorcontrib>Jha, Mithilesh K</creatorcontrib><creatorcontrib>Meissner, Marcel</creatorcontrib><creatorcontrib>Freichel, Marc</creatorcontrib><title>Defective survival of naive CD8 + T lymphocytes in the absence of the β3 regulatory subunit of voltage-gated calcium channels</title><title>Nature immunology</title><addtitle>Nat Immunol</addtitle><description>T cell activation triggers large calcium fluxes. Flavell and colleagues show tonic calcium signaling via Ca
v
1.4-β3 channels are needed for the survival and homeostasis of naive CD8
+
T cells.
The survival of T lymphocytes requires sustained, Ca
2+
influx–dependent gene expression. The molecular mechanism that governs sustained Ca
2+
influx in naive T lymphocytes is unknown. Here we report an essential role for the β3 regulatory subunit of voltage-gated calcium (Ca
v
) channels in the maintenance of naive CD8
+
T cells. Deficiency in β3 resulted in a profound survival defect of CD8
+
T cells. This defect correlated with depletion of the pore-forming subunit Ca
v
1.4 and attenuation of T cell antigen receptor (TCR)-mediated global Ca
2+
entry in CD8
+
T cells. Ca
v
1.4 and β3 associated with T cell signaling machinery and Ca
v
1.4 localized in lipid rafts. Our data demonstrate a mechanism by which Ca
2+
entry is controlled by a Ca
v
1.4-β3 channel complex in T cells.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Immunology</subject><subject>Infectious Diseases</subject><issn>1529-2908</issn><issn>1529-2916</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNptkMtKw0AUhgdRsFbxCYTZKUjqTG7NLKX1BgU3dR3OTE7SKemkzEwC2fhQPojPZEK1K1fn8n_8nPMTcs3ZjLMoezB6xuciOiETnoQiCAVPT489y87JhXNbxng8T-MJ-VxiicrrDqlrbac7qGlTUgPjZrHM6D1d07rf7TeN6j06qg31G6QgHRqFIzuO318RtVi1NfjG9oOVbI32o9o1tYcKgwo8FlRBrXS7o2oDxmDtLslZCbXDq986JR_PT-vFa7B6f3lbPK4CFYZZFKiMzYXkspBxoSJAwUPJoxLiOGFqDjEmUkHBwkwWw6OpEIKzIk1DlmSIqhDRlNwefJVtnLNY5nurd2D7nLN8jC03Oh9jG8i7A-kGwlRo823TWjMc9w96c0AN-Nbi0fJP_wGJYnmp</recordid><startdate>2009</startdate><enddate>2009</enddate><creator>Badou, Abdallah</creator><creator>Flockerzi, Veit</creator><creator>McRory, John E</creator><creator>Flavell, Richard A</creator><creator>Jha, Mithilesh K</creator><creator>Meissner, Marcel</creator><creator>Freichel, Marc</creator><general>Nature Publishing Group US</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>2009</creationdate><title>Defective survival of naive CD8 + T lymphocytes in the absence of the β3 regulatory subunit of voltage-gated calcium channels</title><author>Badou, Abdallah ; Flockerzi, Veit ; McRory, John E ; Flavell, Richard A ; Jha, Mithilesh K ; Meissner, Marcel ; Freichel, Marc</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2283-c8079b1bdb4dc3ae912b13fa4450c7a4e5bcad028bd152699910d662058eecd93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Immunology</topic><topic>Infectious Diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Badou, Abdallah</creatorcontrib><creatorcontrib>Flockerzi, Veit</creatorcontrib><creatorcontrib>McRory, John E</creatorcontrib><creatorcontrib>Flavell, Richard A</creatorcontrib><creatorcontrib>Jha, Mithilesh K</creatorcontrib><creatorcontrib>Meissner, Marcel</creatorcontrib><creatorcontrib>Freichel, Marc</creatorcontrib><collection>CrossRef</collection><jtitle>Nature immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Badou, Abdallah</au><au>Flockerzi, Veit</au><au>McRory, John E</au><au>Flavell, Richard A</au><au>Jha, Mithilesh K</au><au>Meissner, Marcel</au><au>Freichel, Marc</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Defective survival of naive CD8 + T lymphocytes in the absence of the β3 regulatory subunit of voltage-gated calcium channels</atitle><jtitle>Nature immunology</jtitle><stitle>Nat Immunol</stitle><date>2009</date><risdate>2009</risdate><volume>10</volume><issue>12</issue><spage>1275</spage><epage>1282</epage><pages>1275-1282</pages><issn>1529-2908</issn><eissn>1529-2916</eissn><abstract>T cell activation triggers large calcium fluxes. Flavell and colleagues show tonic calcium signaling via Ca
v
1.4-β3 channels are needed for the survival and homeostasis of naive CD8
+
T cells.
The survival of T lymphocytes requires sustained, Ca
2+
influx–dependent gene expression. The molecular mechanism that governs sustained Ca
2+
influx in naive T lymphocytes is unknown. Here we report an essential role for the β3 regulatory subunit of voltage-gated calcium (Ca
v
) channels in the maintenance of naive CD8
+
T cells. Deficiency in β3 resulted in a profound survival defect of CD8
+
T cells. This defect correlated with depletion of the pore-forming subunit Ca
v
1.4 and attenuation of T cell antigen receptor (TCR)-mediated global Ca
2+
entry in CD8
+
T cells. Ca
v
1.4 and β3 associated with T cell signaling machinery and Ca
v
1.4 localized in lipid rafts. Our data demonstrate a mechanism by which Ca
2+
entry is controlled by a Ca
v
1.4-β3 channel complex in T cells.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><doi>10.1038/ni.1793</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Nature immunology, 2009, Vol.10 (12), p.1275-1282 |
| issn | 1529-2908 1529-2916 |
| language | eng |
| recordid | cdi_crossref_primary_10_1038_ni_1793 |
| source | Nature; Springer Nature - Complete Springer Journals |
| subjects | Biomedical and Life Sciences Biomedicine Immunology Infectious Diseases |
| title | Defective survival of naive CD8 + T lymphocytes in the absence of the β3 regulatory subunit of voltage-gated calcium channels |
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