Positioned at the key interface between the blood and tissues, the endothelium normally resists prolonged contact with the leucocytes that abound in blood that bathes the intimal surface.3,24 Stationed as the sentinel, the endothelium serves as the portal governing the entry of leucocytes into tissues to combat invaders, microbial or viral, and to help repair injury and heal wounds. The interplay of the endothelium with leucocyte mediators of innate and adaptive immunity depends on a series of leucocyte adhesion molecules expressed at negligible levels under physiological circumstances. Members of the selectin class of leucocyte adhesion molecules slow the transit of blood leucocytes past the endothelial surface by mediating rolling of these cells. E-selectin (CD62E) causes polymorphonuclear leucocytes to tarry on the endothelial surface. P-selectin (CD62P) and L-selectin (CD62L) also mediate interaction of the endothelial surface with various classes of blood leucocytes. The elevated expression of these endothelial–leucocyte adhesion molecules depends upon irritative stimuli, principally proinflammatory cytokines such as interleukin-1α (IL-1α) and IL-1β or tumour necrosis factor-α (TNF-α).