Background
Polymorphic light eruption (PLE) has been attributed to type IV, most likely delayed-type hypersensitivity response (adaptive immunity) but little is known on innate immunity, especially antimicrobial peptides (AMPs) in the disease. Abnormalities in AMP expression have been linked to pathological skin conditions such as atopic dermatitis (AD) and psoriasis.
Conclusion
The unique profile of differentially expressed AMPs in PLE implies a role in the pathophysiology of the disease, possibly directly or indirectly linked to the microbiome of the skin.
Methods
Antimicrobial peptide profiling was carried out in PLE skin samples (n,12) compared with that of healthy (n,13), atopic (n,6), and psoriatic skin (n,6).
Results
Compared to healthy skin, we observed increased expression of psoriasin and RNAse7 (both mostly in stratum granulosum of the epidermis), HBD-2 (in the cellular infiltrate of the dermis), and LL37 (mostly in and around blood vessels and glands) in PLE lesional skin, a similar expression profile as present in psoriatic skin and different to that of AD (with little or no expression of psoriasin, RNAse7, HBD-2, and LL37). HBD-3 was downregulated in PLE compared to its high expression in the epidermis and dermis of healthy skin, AD, and psoriasis.