# Polymorphic light eruption shows aberrant expression of epidermal tight junction proteins in unexposed and UVR-exposed skin: an experimental study

## TL;DR

This study shows that people with polymorphic light eruption have abnormal skin barrier proteins, both in normal and UV-exposed skin, which may contribute to their condition.

## Contribution

The study reveals novel alterations in tight junction proteins in PLE patients, suggesting a new potential mechanism for the disease.

## Key findings

- Unexposed PLE skin showed significantly lower claudin-1 expression compared to healthy controls.
- UVR exposure in PLE patients altered claudin-7 and claudin-12 expression differently than in healthy skin.
- PLE patients had increased Ki67 expression in unexposed skin, indicating higher cell proliferation.

## Abstract

Polymorphic light eruption (PLE) is a common photodermatosis which is believed to be attributable to an immune reaction to an unidentified photoantigen. The epidermal barrier deters skin entry of photoantigens, but its potential contribution to PLE pathogenesis is unexplored. Our objective was to examine the expression of key barrier proteins in PLE patients in vivo compared with healthy controls, both at baseline and after ultraviolet radiation (UVR) exposure. Seven PLE patients and 10 healthy volunteers were recruited. Small areas of buttock skin were exposed to 80 mJ/cm2 erythemally-weighted UVR (Philips TL12 broadband UVB source, 280–400 nm) and biopsies were taken at 24 h post-UVR and from unexposed buttock skin. Skin sections were assessed by immunostaining for expression of barrier proteins (claudins-1, -4, -7, -12; occludin, filaggrin, loricrin and involucrin), and the proliferation marker Ki67. It was demonstrated that unexposed skin from PLE patients had remarkably lower claudin-1 expression versus healthy volunteers (P < 0.001), while expression of Ki67 was significantly increased. UVR-exposure of healthy volunteer skin reduced claudin-1 expression at 24 h post-UVR (P < 0.01), while in contrast, UVR-exposure of PLE patients decreased the expression of claudin-7 and increased the expression of claudin-12 (both p < 0.05). Thus tight junction protein expression is altered in people with PLE, both in baseline skin and in their response to UVR exposure. These novel findings suggest a potential role for tight junction proteins in PLE pathogenesis and warrant further exploration.