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Elevation of intracellular calcium ion (Ca 2+ ) levels is a vital event that regulates T lymphocyte homeostasis, activation, proliferation, differentiation, and apoptosis. The mechanisms that regulate intracellular Ca 2+  signaling in lymphocytes involve tightly controlled concinnity of multiple ion channels, membrane receptors, and signaling molecules. T cell receptor (TCR) engagement results in depletion of endoplasmic reticulum (ER) Ca 2+  stores and subsequent sustained influx of extracellular Ca 2+  through Ca 2+  release-activated Ca 2+  (CRAC) channels in the plasma membrane. This process termed store-operated Ca 2+  entry (SOCE) involves the ER Ca 2+  sensing molecule, STIM1, and a pore-forming plasma membrane protein, ORAI1. However, several other important Ca 2+  channels that are instrumental in T cell function also exist. In this review, we discuss the role of additional Ca 2+  channel families expressed on the plasma membrane of T cells that likely contribute to Ca 2+  influx following TCR engagement, which include the TRP channels, the NMDA receptors, the P2X receptors, and the IP 3  receptors, with a focus on the voltage-dependent Ca 2+  (Ca V ) channels.

Tweeters, Woofers and Horns: The Complex Orchestration of Calcium Currents in T Lymphocytes