Lymphocyte adhesion to psoriatic dermal endothelium: mechanism and modulation.

Psoriasis is characterized by the hyperproliferation of keratinocytes in the epidermis and the accumulation of activated CD4+ T lymphocytes in the upper dermis. We have recently rested the hypothesis that the abnormal endothelial proliferation in the dermal papillae of psoriatic lesions may be mechanistically linked to the expression of endothelial ligands capable of promoting lymphocytes binding and extravasation. The results indicated that specialized endothelial cells lining the post-capillary venules of psoriatic lesions are capable of promoting the selective adherence of human CD4+ T cells and its memory subset. In contrast, B cells, CD8+ T cells, and CD45RA+ T cells are deficient in their capacities to bind. The adhesion process is energy and calcium dependent and involves tissue-specific lymphocyte receptors, with LFA-1 molecules playing an accessory role. We concluded that transformation of the dermal endothelium into a lymphocyte-receptive phenotype by defined growth factors or cytokines may represent a positive feedback mechanism promoting lymphocyte migration into the diseased sites.