T-cells are activated through formation of the immunological synapse (IS) with antigen-presenting cells (APC). Following formation of the IS, Ca influx through Ca released-activated Ca (CRAC) channels is initiated. Sustaining Ca influx by preventing Ca-dependent inactivation of CRAC channels is necessary for efficient activation and proliferation of T-cells. We show that sustained Ca influx in T-cells correlates with a translocation of mitochondria towards the plasma membrane, observing in many cases a preferential movement of mitochondria towards the IS. This movement is controlled in a Ca-dependent manner and involves the motor proteins kinesin and dynein. The decreased distance between mitochondria and plasma membrane allowed mitochondria to take up large amounts of inflowing Ca, thereby preventing Ca-dependent CRAC channel inactivation. Inhibition of mitochondrial translocation to the plasma membrane significantly reduced either sustained Ca signals or Ca current through CRAC channels. We propose therefore that formation of IS enhances T-cell activation efficiency by moving mitochondria closer to CRAC channels which in turn sustain Ca influx for an extended period. This CRAC channel-mitochondria coupling is augmented by a dramatic cell shape change after formation of IS.