Abstract
As early as 1942, Epstein suggested a photoallergic concept for photodermatoses [s1]. Since then much progress has been made in understanding the pathophysiology of photodermatoses and their most common form, polymorphic light eruption (PLE) (1) (s2-s13). However, specific photoantigens that initiate PLE have not yet been identified. We hypothesize that PLE may be initiated by elements resulting from UV-induced damage to microbial communities of the skin, leading to a cascade of events eventually resulting in the skin rash of the disease.
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