Abstract
The primary trigger of polymorphic light eruption (PLE) remains to be uncovered. 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. One mechanism by which epidermal injury by UV radiation could trigger PLE are danger signals such as damage or pathogen associated molecular patterns DAMP/PAMPs or commensal-associated molecular patterns (CAMPs). Such triggers could be produced due to UV-induced stress on microbial communities of the skin and exacerbate inflammatory responses by inducing the innate immune system through antimicrobial peptides (AMPs) such as psoriasin, RNase7, HBD-2 and LL-37. These AMPs also actively take part in initiating adaptive immunity. That signals derived from microbial rather than human elements may initiate PLE is supported by series of observations, including the PLE-protective effect of topically applied microbial-derived DNA repair enzymes.