Working model showing how DC actin dynamics regulates DC–T cell contact time and priming efficiency. Center: Actin dynamics in WT DCs is regulated by WAVE and WASP in a way that allows for transiently stable DC–T cell contacts, mediated by the pERM–ICAM1–LFA-1 axis, which leads to the activation of a large number of T cells. Right: In the absence of DC WAVE, lateral actin dynamics is reduced, and the altered actin network serves as an ideal substrate for ERM proteins. This leads to an increase in pERM/ICAM1/LFA-1–mediated cell–cell adhesion and allows for the activation of only few T cells compared with WT. Left: in the absence of WASP, actin dynamics at the synapse increases, leading to destabilization of the cell–cell contact and a decrease in interaction time that results in insufficient T cell activation. KO, knockout.