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

Abstract:

: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.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

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

doi

10.1038/ni.1793

subject

Has Abstract

pub_date

2009-12-01 00:00:00

pages

1275-82

issue

12

eissn

1529-2908

issn

1529-2916

pii

ni.1793

journal_volume

10

pub_type

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