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Lymphocyte binding to vascular endothelium in inflamed skin revisited: a central role for vascular adhesion protein‐1 (VAP‐1)

The binding of leukocytes to vascular endothelium and their migration into tissues is mediated by adhesion molecules on the endothelial cells and leukocytes. Vascular adhesion protein‐1 (VAP‐1) is a 170–180/90‐kDa endothelial molecule expressed most prominently in high endothelial venules in peripheral lymph node (PLN) type lymphatic tissues. VAP‐1 mediates lymphocyte binding to PLN, tonsil and synovium. The expression of VAP‐1 is induced in inflammatory diseases such as arthritis and gut inflammation. We examined the expression, structure and function of VAP‐1 in normal and inflamed skin and compared it to those of other adhesion molecules implicated in skin homing. In psoriasis, lichen ruber planus, pemphigoid and allergic lesions, VAP‐1 was markedly up‐regulated. The expression of VAP‐1 was also increased in biopsies of healthy skin of the patients. The VAP‐1 molecule induced in skin is decorated with abundant sialic acids. VAP‐1 in inflamed skin is functional, since inhibition with anti‐VAP‐1 monoclonal antibodies caused a 60% reduction in lymphocyte adhesion to vascular endothelium. Antibodies against E‐selectin, which has been regarded as the major vascular addressin directing cutaneous lymphocyte traffic, and, surprisingly, against peripheral lymph node addressin (PNAd), caused inhibitions of 30% and 60%, respectively, in the frozen section adhesion assay. These findings suggest important roles also for VAP‐1 and PNAd in lymphocyte homing into inflamed skin.