LESIONAL PSORIATIC EPIDERMIS DISPLAYS REDUCED NEUROFIBROMIN IMMUNOREACTIVITY

Neurofibromin enhances the inactivation of protooncogene p2lvas and ha s been suggested to function as a regulator of cell growth and differe ntiation, In normal skin, neurofibromin is particularly abundant in th e basal keratinocytes of epidermis, The present study utilized antibod ies raised against two synthetic peptides corresponding to different r egions of neurofibromin. One of the antibodies recognized all forms of neurofibromin and the other was specific for type II neurofibromin. T he following specimens were analyzed for neurofibromin immunoreactivit y: 1) skin of apparently healthy volunteers, 2) active lesions of 15 p soriatic patients, 3) apparently healthy skin of the same patients at the time of the active phase of the disease, and 4) the previously les ional areas after anti-psoriatic treatment of the same patients, The p resence of neurofibromin mRNA in normal epidermis and in keratinocytes cultured from normal skin was demonstrated by reverse transcriptase-p olymerase chain reaction or by Northern hybridization, In marked contr ast to normal epidermis, active psoriatic lesions were characterized b y a weak immunosignal for types I and II neurofibromin in the basal ce ll layer of the epidermis, Previously lesional, clinically healed area s displayed variable, yet clearly detectable, expression of neurofibro min. Our results demonstrate that the epidermis of psoriatic lesions d isplays reduced immunostaining for type I and Il neurofibromins compar ed to normal epidermis, and that neurofibromin immunoreactivity is par tially restored concomitant with clinical healing of the lesions. The question whether the changes in neurofibromin expression in psoriasis are causal or consequential with respect to the pathogenesis of psoria sis remains to be elucidated.