Abstract
Psoriasis is a chronic inflammatory papulosquamous disease
characterized by multiple remissions and relapses. For long, it was believed to
be primarily a disorder of keratinization. However, the successful use of
traditional immunosupressants and newer immunomodulatory agents in the
treatment of psoriasis led to
the belief that psoriasis is
primarily a disease of Th1 cell immune dysregulation. Recent developments have
brought up several new findings such as the role of Th17 cells and evidence of
skin barrier dysfunction in psoriasis, akin to atopic dermatitis. The present review
aims to focus on these new developments and explain the pathogenesis of psoriasis on the basis of currently available
information.