Abstract

Our knowledge of the pathogenesis and pathologic mechanisms involved in psoriasis has increased greatly over the past few years. Currently, 10 genetic susceptibility variants have been shown to predispose to psoriasis. Although work is being done to determine the biological function of these risk variants and how they predispose to psoriasis, there is no concise model that discusses the role of HLA-Cw6, the strongest risk variant identified to date, or CD8+ T cells, which are the predominant T-cell type in the epidermis of psoriatic lesions. Here, we discuss the relatively unexplored role of CD8+ T cells in psoriasis, their potential interaction with HLA-Cw6 and how this T-cell population may be the main culprit and driving force behind psoriasis. The evidence for involvement of the CD8+ T-cell subset is becoming increasingly convincing and may ultimately lead to better understanding of the autoimmune basis of psoriasis and eventual cure of this disease.

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