ICAM-1 engagement controls hepatic cell polarity, but this receptor can also signal without prior leukocyte interaction, thanks to its confinement into apical, microvilli-enriched, bile-canalicular domains and its actin connector EBP50.

Loss of membrane-bound ICAM-1, overexpression of soluble ICAM-1 or ILKAP activity in tumor cells induce resistance to antigen-specific cytotoxic T-cell-mediated killing independently from regulating antigen presentation, PD-L1 expression, IFN-γ, or TNF-α responsiveness.

Mammary progenitors identified by a new marker, ICAM-1, undergo epithelial-mesenchymal transition and luminal-to-basal switch in response to paracrine Met activation.

B-cell integrin co-stimulation promotes the formation of an actomyosin network that drives integrin-dependent immune synapse formation and B-cell activation.

Protein repairing enzyme PIMT maintains vascular endothelium in a quiescent state, thus preventing the development of inflammatory vascular diseases.

TCR and CD40L microclusters are linked in synaptic ectosomes (extracellular vesicles) and released in the immunological synapse by helper T cells and induce dendritic cell maturation and cytokine production.

Inhibition of the catalytic activity of the Zap70 kinase reveals that discrete TCR-regulated events control the remodelling of the actin cytoskeleton when the cytotoxic T cell interacts with its target.

Reactive endothelial venules are a new vessel subtype characterized by consistent expression of cell adhesion molecules, preferential leukocyte transmigration, association with perivascular macrophages, and the initiation of CNS immune responses.

A lipid mediator lysophosphatidic acid (LPA) derived from fibroblastic reticular cells regulates T-cell movement through the densely packed reticular network in lymph nodes in a manner dependent on the LPA receptor LPA₂-ROCK-myosin II.

The strength of TCR signalling determines the rate at which cells initiate a tightly coordinated signalling programme, without altering its organization.