Abstract
Calcium (Ca2+) is a universal second messenger important for T lymphocyte homeostasis, activation, proliferation, differentiation, and apoptosis. The events surrounding Ca2+ mobilization in lymphocytes are tightly regulated and involve the coordination of diverse ion channels, membrane receptors, and signaling molecules. A mechanism termed store-operated Ca2+ entry (SOCE), causes depletion of endoplasmic reticulum (ER) Ca2+ stores following T cell receptor (TCR) engagement and triggers a sustained influx of extracellular Ca2+ through Ca2+ release-activated Ca2+ (CRAC) channels in the plasma membrane. The ER Ca2+ 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 Ca2+ channels expressed on the plasma membrane of T cells that likely contribute to Ca2+ influx following TCR engagement, particularly highlighting an important role for voltage-dependent Ca2+ channels (CaV) in T lymphocyte biology.
Highlights
Calcium (Ca2+) is a universal second messenger important for T lymphocyte homeostasis, activation, proliferation, differentiation, and apoptosis
We review the role of several additional families of Ca2+ channels expressed on the plasma membrane of T cells that likely contribute to Ca2+ influx following T cell receptor (TCR) engagement, highlighting an important role for voltage-dependent Ca2+ channels (CaV) in T lymphocyte biology
In the body’s steady-state, a pool of T lymphocytes that express a diverse T cell receptor (TCR) repertoire is maintained in the periphery
Summary
2005; Smith-Garvin et al, 2009). Ca2+ has been proposed to regulate the Ras/mitogen-activated protein kinase (MAPK) pathway in T cells. STIM1-deficient T cells have no CRAC channel function or SOCE, no subsequent activation of NFAT transcription factor and, as a result, have impaired cytokine secretion (Oh-Hora et al, 2008). This impacts T cell responses and, confers protection from experimental autoimmune encephalomyelitis (EAE) due to poor generation of Th1/Th17 responses (Schuhmann et al, 2010). Further work is required to clearly fit the IP3R into the Ca2+ signaling network in T cells
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