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A dermal lymphocytic infiltrate is a characteristic feature of psoriasis, and may be involved in the pathogenesis of the disease. We have previously shown that specialized dermal microvascular endothelial cells (DMEC) in psoriatic lesions promote the selective adherence of the CD4 CD45Ro helper T-cell subset. In this study, we examined the adhesive interaction between peripheral blood mononuclear cells and psoriatic DMEC in patients treated with ultraviolet B light (UVB), and correlated the results with the expression and function of endothelial adhesion molecules on DMEC. Seven psoriatic patients were exposed to one MED of UVB daily for 14 days, and the binding properties of their peripheral blood mononuclear cells (PBMC), and tissue specimens taken from their lesions on days 0, 2, 3, 6, 8, 11 and 14 of UVB treatment, were studied. The ability of psoriatic PBMC to adhere to non-irradiated control or UVB-treated psoriatic plaques was reduced by 70% after treatment with 2-3 MED, and complete inhibition was obtained after 8-11 MED. In contrast, exposure of psoriatic plaques to 2-3 MED had no effect on the capacity of DMEC to support normal PBMC binding, which was only reduced after 8-11 MED. In addition, psoriatic plaques which were shielded from direct UVB exposure also showed decreased PBMC binding, suggesting a systemic effect of UVB treatment. Immunoperoxidase staining revealed that CD54 (ICAM-1) and E-selectin were strongly expressed on dermal vessels in untreated psoriatic plaques. Treatment of patients with 6-8 MED significantly decreased CD54 and E-selectin expression. In contrast, VCAM-1 expression on untreated plaques was weaker than that of CD54 and E-selectin, but was markedly induced following UVB treatment. In functional blocking studies, preincubation of tissue from untreated psoriatic plaques with anti-E-selectin antibody, but not antibodies against CD54 and VCAM-1, significantly inhibited the ability to bind normal PBMC. These observations suggest that UVB treatment interferes with the adhesive properties of both psoriatic PBMC and endothelial cells, and differentially regulates the expression of endothelial adhesion molecules. The study also provided direct evidence for the involvement of E-selectin in the adhesion of circulating lymphocytes to psoriatic endothelial cells.

A dermal lymphocytic infiltrate is a characteristic feature of psoriasis, and may be involved in the pathogenesis of the disease. We have previously shown that specialized dermal microvascular endothelial cells (DMEC) in psoriatic lesions promote the selective adherence of the CD4 CD45Ro helper T-cell subset. In this study, we examined the adhesive interaction between peripheral blood mononuclear cells and psoriatic DMEC in patients treated with ultraviolet B light (UVB), and correlated the results with the expression and function of endothelial adhesion molecules on DMEC. Seven psoriatic patients were exposed to one MED of UVB daily for 14 days, and the binding properties of their peripheral blood mononuclear cells (PBMC), and tissue specimens taken from their lesions on days 0, 2, 3, 6, 8, 11 and 14 of UVB treatment, were studied. The ability of psoriatic PBMC to adhere to non-irradiated control or UVB-treated psoriatic plaques was reduced by 70% after treatment with 2-3 MED, and complete inhibition was obtained after 8-11 MED. In contrast, exposure of psoriatic plaques to 2-3 MED had no effect on the capacity of DMEC to support normal PBMC binding, which was only reduced after 8-11 MED. In addition, psoriatic plaques which were shielded from direct UVB exposure also showed decreased PBMC binding, suggesting a systemic effect of UVB treatment. Immunoperoxidase staining revealed that CD54 (ICAM-1) and E-selectin were strongly expressed on dermal vessels in untreated psoriatic plaques. Treatment of patients with 6-8 MED significantly decreased CD54 and E-selectin expression. In contrast, VCAM-1 expression on untreated plaques was weaker than that of CD54 and E-selectin, but was markedly induced following UVB treatment. In functional blocking studies, preincubation of tissue from untreated psoriatic plaques with anti-E-selectin antibody, but not antibodies against CD54 and VCAM-1, significantly inhibited the ability to bind normal PBMC. These observations suggest that UVB treatment interferes with the adhesive properties of both psoriatic PBMC and endothelial cells, and differentially regulates the expression of endothelial adhesion molecules. The study also provided direct evidence for the involvement of E-selectin in the adhesion of circulating lymphocytes to psoriatic endothelial cells.

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