Is psoriasis a T-cell disease?

The etiology and pathogenesis of psoriasis - one of the most common chronic , inflammatory, hyperproliferative skin disorders of man - have long fascin ated dermatologists, pathologists and biologists alike. Here, we have a mod el disease that offers to study neuroectodermal-mesenchymal interactions in the widest sense possible. Epithelial, endothelial, and hematopoietic cell s as well as neurons projecting into the skin apparently all interact with each other to generate the characteristic psoriatic lesion. For decades, th e ongoing controversy on the molecular nature, choreography and hierarchy o f these complex interactions e.g. between epidermal keratinocytes, T cells, neurotrophils, endothelial cells and sensory nerves has served as a drivin g force propelling investigative dermatology to ever new horizons. This deb ate has not only been at the heart of our quest to develop more effective f orms of therapy for this socially crippling disease, but it also has profou ndly influenced how we view the skin as a whole: the numerous competing the ories on the pathogenesis of psoriasis published so far also are reflection s on the evolution of mainstream thought in skin biology over the last deca des. These days, conventional wisdom infatuated with a T-cell-centered appr oach to inflammatory skin diseases - portrays psoriasis as an autoimmune di sease, where misguided T lymphocyte activities cause secondary epithelial a bnormalities. And yet, as this CONTROVERSIES feature reminds us, some autho ritative "pockets of academic resistance" are still quite alive, and interp ret psoriasis e.g. as a genetically determined, abnormal epithelial respons e pattern to infectious and/or physicochemical skin insults. Weighing the c orresponding lines of argumentation is not only an intriguing, clinically r elevant intellectual exercise, but also serves as a wonderful instrument fo r questioning our own views of the skin universe and its patterns of deviat ion from a state of homeostasis.