The expression of 65 kiloDalton heat shock protein (HSP65) immunoreactivity of skin biopsies from experimentally induced polymorphic light eruption (PLE) lesions was studied, to investigate its possible role as a photo-induced antigen responsible for precipitating lesions. In each subject the 24-h minimal erythema dose of solar simulated radiation was determined and an area of skin previously affected by PLE subjected to 70% of the minimal erythema dose in order to induce PLE lesions. The irradiated areas were sequentially biopsied between 0 and 6 days. ML-30, a monoclonal antibody which recognises heat shock protein 65, was used to label the sections by means of an indirect immunoperoxidase technique. In PLE patients clinical inflammation was noted by 5 h post-irradiation, with subsequent evolution of PLE-like lesions; these were still present at 6 days. Increased ML-30 antibody labelling in epidermal keratinocyte and endothelial cell cytoplasm was recognisable from 1 h post-irradiation, and in dermal dendritic cells from 5 h sustained through to 6 days. In normal subjects neither clinical nor histological features of inflammation were noted after irradiation, nor any increase in HSP65 labelling.
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A 1994 study studied this question.