In reply
I am intrigued by the observations of Professor Jablonska and her colleagues in France and Poland regarding the possible role of specific strains of HPV in the pathogenesis of psoriasis. As noted by the authors, I have proposed a novel hypothesis (published in both a brief1 and extended commentary2) conceived around the notion that formation of a psoriatic plaque represents a cutaneous innate immune response that culminates in a protective shield from infectious agents. One can explain the induction of cytokines and costimulatory molecules and even the recruitment of NK-T cells as the psoriatic cutaneous response to the presence of a pathogen on the skin.3 From this perspective, it is perhaps not a coincidence that some patients with psoriasis possess a genetically predetermined susceptibility to a specific strain of HPV that would foil the best attempts of the innate and adaptive immune responses to combat such an infectious agent.