A sustained Ca2؉ entry is the primary signal for T lymphocyte activation after antigen recognition. This Ca 2؉ entry mainly occurs through store-operated Ca 2؉ channels responsible for a highly selective Ca 2؉ current known as I CRAC . Ca 2؉ ions act as negative feedback regulators of I CRAC , promoting its inactivation. Mitochondria, which act as intracellular Ca 2؉ buffers, have been proposed to control all stages of CRAC current and, hence, intracellular Ca 2؉ signaling in several types of non-excitable cells. Using the whole-cell configuration of the patch clamp technique, which allows control of the intracellular environment, we report here that respiring mitochondria located close to CRAC channels can regulate slow Ca 2؉ -dependent inactivation of I CRAC by increasing the Ca 2؉ -buffering capacity beneath the plasma membrane, mainly through the release of ATP.

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