Figure 2.

Distinct intracellular compartments control TCR, LAT, and Lck exocytosis. Regulated exocytosis of receptors and signaling molecules is initiated upon TCR activation. According to current understanding, exocytosis of the TCR-CD3 complex is mainly facilitated by newly formed Rab8- and Rab3-positive vesicles. Fast (Rab4-positive vesicles) and slow (Rab11-positive vesicles) recycling compartments can also contribute to the delivery of the TCR-CD3 complex to the immunological synapse. Lck co-localizes with Rab11-positive vesicles. LAT vesicles mainly contain the late endosome/lysosome markers of Rab27 and Rab37 but LAT also co-localizes with newly synthesized Rab8-positive vesicles. There appears to be little overlap between the TCR, LAT, and Lck exocytic trafficking pathways, indicating that distinct trafficking routes of signaling molecules may facilitate segregation before stimulation, and efficient delivery to and high number of encounters within the immunological synapse after stimulation. EE, early endosome; LE, late endosome; RE, recycling endosome; SV, secreting vesicle.