Psoriasis is a chronic, relapsing, immune-based skin disease that affects an estimated 1-3% of the world's population.1 There is no consensus regarding the exact etiology of psoriasis; among several postulated pathophysiological causes, excessive activity of T cell-mediated immune response, and T-helper (Th) in particular, is the most accepted theory. This is supported by increased levels of pro-inflammatory cytokines, especially tumor necrosis factor (TNF-α) in the serum, skin lesions and joints of these patients.2,3