Model showing how DCs regulate ICAM-1 mobility to enhance LFA-1 activation on T cells. (left) In immature DCs, levels of active moesin and α-actinin are low, allowing significant lateral mobility of ICAM-1. Upon maturation (right), moesin and α-actinin are up-regulated and activated, leading to immobilization of ICAM-1 via interactions between the cytoskeleton and the ICAM-1 cytoplasmic tail. Low-mobility ICAM-1 provides increased resistance to forces applied to the LFA-1 β-chain by the T cell actin cytoskeleton. This process promotes LFA-1 tail separation, and conformational changes in the extracellular domain associated with increased affinity for ICAM-1. Ultimately, these events lead to increased adhesion and T cell activation.