Aberrant Gene Expression With Deficient Apoptotic Keratinocyte Clearance May Predispose To Polymorphic Light Eruption

Polymorphic light eruption (PLE) is the commonest photodermatosis, demonstrating intermittently appearing non-scarring pruritic, erythematous papules, vesicles or plaques on patient skin within hours of ultraviolet radiation (UVR) exposure. It depends on genetic susceptibility as well as environmental UVR exposure and is apparently a failure of normal UVR-induced immunosuppression in the presence of simultaneously produced skin photoneoantigens1,2, with a resulting increased immune response. Reduced TNF-α, IL-4 and IL-10 expression, a lack of neutrophils, reduced T-helper-1/T-helper-2 skewing and reduced Langerhans cell migration have also been demonstrated in UVB-irradiated PLE skin3. Bead-array immunoassay studies have further revealed significantly higher PLE baseline IL-1β and CCL11 (eotaxin) spring plasma levels4, while decreased TGFs1, IL-10 and receptor activator of nuclear factor kappa-B ligand (RANKL) epidermal and dermal expression, and reduced T-reg cells occur in UVA-1-irradiated patients5, as well as decreased T-reg cell function in all PLE patients, irradiated or not6.This article is protected by copyright. All rights reserved.