"Leukocyte trafficking "

     TIn several pathophysiological conditions, inflammatory cells (e.g. leukocytes, neutrophils, T-cells) will leave the bloodstream by crossing the endothelial monolayer and migrate into the underlying tissues. It is now clear that the process of extravasation involves a range of adhesion molecules on both circulating and endothelial cells, as well as extensive intracellular signaling that drives adhesion and chemotaxis on the one hand and controls a transient modulation of endothelial integrity on the other. Moreover, chronic inflammatory settings lead to vascular leakage, a hallmark of several diseases where endothelial barrier dysfunction is often the underlying cause. The subsequent stages of endothelial barrier dysfunction contribute to endothelial hyperpermeability. Interestingly, these transendothelial migration and barrier dysfunction primarily occur at the at an specific location, postcapillary venules.