Cell-mediated immunity (CMI) in psoriasis.
Patients with psoriasis were found to have less intensive experimental DNCB sensitization and decreased lymphocyte response to nonspecific mitogens, PHA, Con A, and PWM. E rosette formation was defective only in active psoriasis, in contrast to normal T and B cell counts. A reduction in DNCB hypersensitivity development and the percentage of E rosette forming lymphocytes were related to disease activity, but not to extention of skin lesions. The defect of E rosette function appeared to be transitional and completely disappeared in the remission. Abnormalities in CMI in psoriasis were found to be related at least partially to the existence in patients sera of a factor inhibiting normal T lymphocyte function. The study provides no evidence for the presence of primary CMI defect in psoriasis.
D001402:B-Lymphocytes / Q000276:immunology; D003208:Concanavalin A / Q000494:pharmacology; D003877:Dermatitis, Contact / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D007165:Immunosuppression Therapy; D007958:Leukocyte Count; D011565:Psoriasis / Q000276:immunology*; D012397:Rosette Formation; D013601:T-Lymphocytes / Q000276:immunology
D003208:Concanavalin A