Psoriasis: an epidermal disease after all?

摘要

In the September 15th issue of Nature, a research group from Austria reported a novel mouse model with epidermal specific double-knockout of the c-Jun and JunB genes with subsequent development of psoriasis-like skin phenotypeand arthritic lesions. In this interesting model, the authors show that epidermal changes precede and are independent of recruitment or function of T cells.Psoriasis is a common chronic inflammatory and hyperproliferative skin disease characterized by complex alterationsin epidermal growth and differentiation, as well as multiple inflammatory, immunologicaland vascular abnormalities. A significant proportion of psoriasis patients also develop seronegative inflammatory arthritis. Many lines of evidence indicate that the disease is genetic, although its mode of inheritance is usually multifactorial. To date, no causative gene has been definitively identified.