Cellular autoimmunity in psoriasis and lichen planus

Abstract The objective of this investigation was to determine whether specific cellular recognition of the epidermis is associated with the human skin diseases, psoriasis and lichen planus. Epidermal cells (EC) obtained from biopsies of involved and uninvolved skin of patients with these diseases were used as stimulators and targets for autologous peripheral blood mononuclear cells (PBMC) in assays of three conventional manifestations of cellular immunity: lymphocyte transformation, leukocyte migration-inhibition and cell-mediated cytotoxicity. Parallel tests were conducted with autologous PBMC as stimulators to ascertain the tissue specificity of the reactions evoked by autologous EC. Similar assays were conducted with EC and PBMC from a large group of normal subjects, and the results were compared to those of the dermatology patients by rigorous statistical analyses. No evidence of lymphocyte-mediated cytotoxicity towards autologous EC was obtained with any of the subject groups, but autologous EC, and to a lesser extent PBMC, of the psoriasis patients, but not of the other two groups, evoked significant lymphocyte transformation. These results were obtained only with patients on Goeckerman therapy, raising the possibility that they were a manifestation of the treatment (topical coal-tar and ultraviolet light irradiation) rather than of the disease, although reasons are presented why this is unlikely. Clearer evidence of disease-associated autoimmunity was obtained in the leukocyte migration-inhibition assays, where autologous EC, and to a lesser extent, PBMC, of the psoriasis patients in general, not just those on Goeckerman therapy, and not those of the lichen planus patients or of the normal subjects, stimulated the release of a leukocyte migration-inhibition factor. These results support the concept of a central role for T-cell mediated autoimmunity in the pathogenesis of psoriasis.