Cyclosporin in psoriasis: pathophysiology and experimental data

Abstract

Cyclosporin has been used efficaciously in recent years for the management of severe psoriasis. The remarkable efficacy of this drug and its known immunosuppressive properties have indicated even more strongly the involvement of the immune system in the induction and maintenance of psoriasis. The present review summarizes the role of cellular immunity in the pathogenesis of psoriasis and possible mechanisms of action of cyclosporin in psoriasis, and describes the laboratory studies performed in our Department under two headings, changes in lesional immune infiltrate (evaluated immunohistologically) and changes in neutrophil chemotaxis during cyclosporin treatment. Our immunohistological study showed that the psoriatic plaques contained an infiltrate composed mainly of activated CD4+ T cells. Cyclosporin treatment significantly decreased T cells and normalized the distribution and antigen expression of intraepidermal Langerhans cells, increasing the number of CD1+ dendritic cells. Our studies on neutrophil chemotaxis showed that cyclosporin reduced the chemotactic activity of neutrophilic polymorphonuclear leukocytes (in vivo but not in vitro), seemingly as a consequence of blocking the production of chemoattracting cytokines by psoriatic monocytes.