Fig. 2.

Cell polarity complexes involved in T cell migration. Simplified scheme of a migrating T cell exhibiting a front-rear polarity. T cell polarization starts with the stimulation of chemokine receptors that triggers in turn the activation of adhesion proteins as LFA-1 integrin and actin and microtubule cytoskeleton remodeling, leading to morphological changes. Polarity regulators localizing at the leading edge scaffold various signaling molecules, including the small GTPases Rac1 and Cdc42, ensuring actin and microtubule cytoskeleton balance and the formation of a leading lamellipodium. At the cell rear, a protrusion called uropod forms and concentrates ERM proteins, linking membrane components with the cortical actin cytoskeleton, and adhesions molecules such as CD44, ICAM-1,2,3 that interact with ERMs and integrins, such as LFA-1. RhoA signaling is key to maintain these subcellular organization, while myosin-IIA facilitates contraction of this region thus supporting T cell migration.