Introduction

Abstract

Psoriasis is an immune-mediated skin disease in which T cells initiate and maintain the pathogenic process.¹ T cells become activated, migrate into the skin, and induce the keratinocyte proliferation associated with the psoriatic phenotype. The activated T cells that infiltrate the skin express the memory phenotype (CD45RO⁺).^2,3 Both CD4⁺ and CD8⁺ memory T-cell subtypes are believed to play a role in the pathogenesis of psoriasis. The effectiveness of many traditional therapies for psoriasis (e.g., cyclosporine, methotrexate, psoralen/ultraviolet A light) can be attributed, at least in part, to the potent immunosuppressive effects of these treatments.^4,5 Unfortunately, a lack of selective targeting of the immune system by these therapies may result in treatment-limiting side effects.