Keratin 17: a critical player in the pathogenesis of psoriasis.

Keratin 17 (K17) is an intermediate filament protein present in the basal cells of complex epithelia, such as nails, hair follicles, sebaceous glands, and eccrine sweat glands. Studies have shown that it is expressed aberrantly in the suprabasal keratinocytes of psoriatic lesions, compared to in normal epidermis. K17 is also closely associated with the immune system and plays an important role in the pathogenesis of psoriasis. In this review, we present our experimental findings concerning the role of K17 in psoriasis, and compare them to results published in the literature. Our results show that cytokines related to Th17 and IL-22-producing (where Th17 is T helper cells, type 17 and IL is interleukin) CD4(+) T cells, including IL-17A and IL-22, upregulate the expression of K17 in keratinocytes. In addition, K17 stimulates autoreactive T cells and promotes the production of psoriasis-associated cytokines. Our findings lend support to the hypothesis that a K17/T-cell/cytokine autoimmune loop is involved in the pathogenesis of psoriasis. We therefore review the current understanding of the K17 immunoregulation, including its expression and direct/indirect effects on immune responses. Pertinent strategies for the treatment of psoriasis are also discussed.