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    Nat Immunol. 2009 Dec;10(12):1275-82. Epub 2009 Oct 18.

    Defective survival of naive CD8+ T lymphocytes in the absence of the beta3 regulatory subunit of voltage-gated calcium channels.

    Jha MK, Badou A, Meissner M, McRory JE, Freichel M, Flockerzi V, Flavell RA.

    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.

    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 beta3 regulatory subunit of voltage-gated calcium (Ca(v)) channels in the maintenance of naive CD8(+) T cells. Deficiency in beta3 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 beta3 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-beta3 channel complex in T cells.

    PMID: 19838200 [PubMed - indexed for MEDLINE]

    PMCID: PMC2785134 [Available on 2010/6/1]

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