Dermal lymphocytic infiltrates are characteristic features of psoriasis and may be involved in the pathogenesis of the disease. We have previously shown that specialized endothelial cells are present in the dermis of psoriatic skin and are capable of supporting lymphocyte adherence and promoting lymphocyte extravasation. In this study, we investigated the dermal endothelial binding properties of human lymphocyte subsets and the role of LFA-1 molecules in the adhesion process. It was found that both human T cells and B cells adhered to frozen sections of psoriatic plaques, but with different cell dose-response relationships. In addition, quantitative assessment of lymphocyte adhesion demonstrated that human CD4⁺ T cells and the CDw29⁺ (helper-inducer) subset adhered preferentially to the papillary dermis as compared with CD8⁺ T cells or the CD45R⁺ (suppressor-inducer) subset. Moreover, human lymphocytes adhered to untreated psoriatic plaques, but not to uninvolved skin or to steroid- treated, clinically and histologically resolved lesions. Preincubation of T lymphocytes with saturating amounts of monoclonal antibody 60.3 against the surface membrane CD18 glycoprotein complex inhibited partially their capacity to bind to untreated psoriatic plaques. These observations suggest that the emigration of human CD4⁺ T cell and the CDw29⁺ helper-inducer subset is promoted by selective adherence to psoriatic dermal endothelia, with LFA-1 molecules playing an accessory role in the binding process.