HEAT-SHOCK PROTEIN-65 IMMUNOREACTIVITY IN EXPERIMENTALLY-INDUCED POLYMORPHIC LIGHT ERUPTION

The expression of 65 kiloDalton heat shock protein (HSP65) immunoreact ivity of skin biopsies from experimentally induced polymorphic light e ruption (PLE) lesions was studied, to investigate its possible role as a photo-induced antigen responsible for precipitating lesions. In eac h subject the 24-h minimal erythema dose of solar simulated radiation was determined acid an area of skin previously affected by PLE subject ed 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 immunoperoxidas e technique. In PLE patients clinical inflammation was noted by 5 h po st-irradiation, with subsequent evolution of PLE-like lesions; these w ere still present at 6 days. Increased ML-30 antibody labelling in epi dermal keratinocyte and endothelial cell cytoplasm was recognisable fr om 1 h post-irradiation, and in dermal dendritic cells from 5 h sustai ned through to 6 days. In normal subjects neither clinical nor histolo gical features of inflammation were noted after irradiation, nor any i ncrease in HSP65 labelling.