Effect of Cyclosporine on Peripheral Blood and Lesional Skin in Psoriatic Patients

Posted by James

INTRODUCTION

T cells are thought to play a critical role in the pathogenesis of psoriasis. The tissue-selective homing of T cells to psoriatic skin lesions is regulated primarily by interaction of T cell homing receptors with adhesion molecules on the endothelial cells. The molecules mediating the varied degrees of adhesion between leukocyte and endothelium include the small selectin family which mediates the very early transient adhesions as well as the rolling interactions. Among these, E-selectin is known to be up-regulated on the vascular endothelium of inflammatory skin lesions such as psoriasis. Cu­taneous lymphocyte antigen (CLA) is expressed in a subset of circulating memory T cells and in the majority of skin-infiltrating T cells and is thought to mediate the homing of circulating skin-associated T cells to cutaneous inflammatory sites by in­teracting with endothelial cell ligand E-selectin. The immunosuppressive effect of cyclosporine is mediated by the inhibition of IL-2 production by activated T cells. Cyclosporine downregulates the expression of ICAM-1 and E-selectin on the endothelial cells and reduces the number of CD4+ and CD8+ T cells in dermal infiltrates. The tissue- selective homing of memory T cells in psoriatic lesions is regulated primarily by interaction of T-cell homing receptors with vascular adhesion molecules. In psoriatic skin lesions, the number of CLA T cells and expression of Е-selectin on the endothelial cells were increased, CLA / E-selectin is critical for trafficking skin-associated T cells to psoriatic skin lesions. We examined the effect of cyclosporine on expression of E-selectin on psoriatic lesional endothelial cells and also evaluated E-selectin immunohistochemical expression in recurrent lesions. We also examined the effect of cyclosporine on CLA+ T cells in peripheral blood using FACS analysis. erectalis 20 mg