| GETTING TO GRIPS WITH PSORIASISThe stage set to unfold before us the fascinating pathophysiology of psoriasis is ever changing. Some of the actors have added intriguing insight to our understanding of this complex inflammatory disorder.Formerly, psoriasis had been regarded as a skin disease that is based primarily on disturbances of epidermal homeostasis.1,2 In fact, even in more recent times there are some absolutely serious "pockets of resistance" providing experimental evidence that a primary epithelial abnormality alone can initiate psoriasis-like hyperproliferative inflammatory skin changes, at least in animal models. 3,4 Alas, as this is a viewpoint article, we dare to phrase the "heretic" notion that tampering with almost any component of the cutaneous environment, be it epithelium, vasculature or immune functions, can ultimately result in so-called psoriasiform inflammation. 5 The predominant current scenario, however, which is substantiated quickly by even a cursory survey of the literature, is this: psoriasis is a systemic inflammatory disorder, has an immunogenetic basis and is centred around tightly intertwined interactions of the innate and the adaptive immune system.
6-11More than 18 000 publications pertaining to the pathogenesis of