Ros A M, Wennersten G
Department of Dermatology, Karolinska Hospital, Stockholm, Sweden.
Photodermatol. 1987 Apr;4(2):79-87.
To gain further insight into the pathogenesis of photosensitive psoriasis, i.e. worsening of psoriasis lesions after sun exposure, 21 patients with this condition were studied following provocation with high doses of UVA and UVB. Thirteen of the patients had a history of polymorphous light eruption (PMLE). Here, a PMLE reaction could be induced by UV provocation. In 7 cases this developed further into psoriasis. In 8 of the 21 patients, psoriatic lesions developed subsequent to provocation with no preceding PMLE reaction. The test areas were periodically biopsied, and processed with a two-stage immunoperoxidase technique using monoclonal antibodies to immunophenotype the cell infiltrate. The dermal infiltrate consisted mainly of Leu-4+ cells (PAN-T). Leu-3+ cells (T-helper/inducer phenotype) dominated, with a smaller proportion of Leu-2+ cells (T-cytotoxic/suppressor phenotype), except in a few cases where these were prominent. This pattern was seen in all the groups investigated, including a control group of non-psoriatic PMLE patients. Exocytosis, with mainly Leu-2+ cells in the epidermis, was seen in most patients after psoriasis had developed. OKT-6+ (Langerhans) cells in the dermis were sparse, except in a few patients in all groups where a considerable number were observed. Leu-M1+ cells in the dermis (monocytes, granulocytes) were also sparse, but increased in most patients after psoriasis had developed. No B1+ cells (B lymphocytes) were seen, and very few Leu-7+ cells (NK). The only significant differences in the reaction pattern between the different clinical groups were the increased number of Leu-M1+ cells and the exocytosis of Leu-2+ cells after psoriasis had developed.