Aberrant gene expression with deficient apoptotic keratinocyte clearance may predispose to polymorphic light eruption

Abstract

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 photoneoantigens^1,2, 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 TGFß1, 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.

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