Heat shock protein 65 immunoreactivity in experimentally induced polymorphic light eruption.

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.