Defective survival of naive CD8+ T lymphocytes in the absence of the β3 regulatory subunit of voltage-gated calcium channels
Copyright policy )Defective survival of naive CD8+ T lymphocytes in the absence of the β3 regulatory subunit of voltage-gated calcium channels
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.
- University of Calgary Canada
- School of Medicine Yale University United States
- Yale University United States
- Cadi Ayyad University Morocco
- University of Calgary, Hotchkiss Brain Institute Canada
Mice, Knockout, Calcium Channels, L-Type, Cell Survival, Apoptosis, CD8-Positive T-Lymphocytes, Immunity, Innate, Mice, Gene Expression Regulation, Animals, Homeostasis, Calcium Channels, Calcium Signaling, fas Receptor
Mice, Knockout, Calcium Channels, L-Type, Cell Survival, Apoptosis, CD8-Positive T-Lymphocytes, Immunity, Innate, Mice, Gene Expression Regulation, Animals, Homeostasis, Calcium Channels, Calcium Signaling, fas Receptor
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