Activation-induced expression of non-muscle myosin IIB shapes T cell polarity and the immune synapse
Speaker: María Millán Salanova
Centro de Investigación del Cáncer (CIC-IBMCC)
Salón de actos del Centro de Investigación del Cáncer
In this study, we describe that the B paralog of non-muscle myosin II (NMII-B) is a key component of the mechanosensitive machinery that controls the interaction of the T cell with antigen-presenting cells. siRNA studies on flat surfaces combined with models of antigenic stimulation revealed that NMII-B-depleted human primary CD4+ T cells and leukemic T cells lose contact inhibition of protrusion as they interact with the surface of the APC, generating over-extended T: APC interfaces with an abnormal localization of the components of the supramolecular activation clusters. These defects, due to unconstrained actin polymerization at the edge of the T: APC interface, decrease T cell activation. In addition, NMII-B controls T cell polarization and migration. These effects are important in activated T cells, which express higher levels of NMII-B than nonactivated cells. Together, these results position NMII-B as a novel effector that mediates the efficient activation and increased motility of effector T cells.