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Front Immunol. 2013 Jun 24;4:164. doi: 10.3389/fimmu.2013.00164. eCollection 2013.

Weft, warp, and weave: the intricate tapestry of calcium channels regulating T lymphocyte function.

Author information

1
Michael Smith Laboratories, University of British Columbia , Vancouver, BC , Canada ; Centre for Blood Research, University of British Columbia , Vancouver, BC , Canada ; The Brain Research Centre, University of British Columbia , Vancouver, BC , Canada ; Department of Microbiology and Immunology, University of British Columbia , Vancouver, BC , Canada ; Department of Medical Genetics, University of British Columbia , Vancouver, BC , Canada ; Department of Zoology, University of British Columbia , Vancouver, BC , Canada.

Abstract

Calcium (Ca(2+)) is a universal second messenger important for T lymphocyte homeostasis, activation, proliferation, differentiation, and apoptosis. The events surrounding Ca(2+) mobilization in lymphocytes are tightly regulated and involve the coordination of diverse ion channels, membrane receptors, and signaling molecules. A mechanism termed store-operated Ca(2+) entry (SOCE), causes depletion of endoplasmic reticulum (ER) Ca(2+) stores following T cell receptor (TCR) engagement and triggers a sustained influx of extracellular Ca(2+) through Ca(2+) release-activated Ca(2+) (CRAC) channels in the plasma membrane. The ER Ca(2+) sensing molecule, stromal interaction molecule 1 (STIM1), and a pore-forming plasma membrane protein, ORAI1, have been identified as important mediators of SOCE. Here, we review the role of several additional families of Ca(2+) channels expressed on the plasma membrane of T cells that likely contribute to Ca(2+) influx following TCR engagement, particularly highlighting an important role for voltage-dependent Ca(2+) channels (CaV) in T lymphocyte biology.

KEYWORDS:

L-type calcium channels; T cell; T cell signaling; calcium; calcium channels

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