Differential Expression of Cytokines in UV-B–Exposed Skin of Patients With Polymorphous Light Eruption

Abstract

<h3>Background</h3> Disturbances in UV-induced Langerhans cell migration and T helper (T_H) 2 cell responses could be early steps in the pathogenesis of PLE. <h3>Objective</h3> To establish whether UV-B exposure induces aberrant cytokine expression in the uninvolved skin of patients with polymorphous light eruption (PLE). <h3>Design</h3> Immunohistochemical staining and comparison of microscopic sections of skin irradiated with 6 times the minimal dose of UV-B causing erythemaand the unirradiated skin of patients with PLE and of healthy individuals. <h3>Setting</h3> University Medical Center (Dutch National Center for Photodermatoses). <h3>Patients</h3> Patients with PLE (n = 6) with clinically proven pathological responses to UV-B exposure and normal erythemal sensitivity. Healthy volunteers (n =5) were recruited among students and hospital staff. <h3>Main Outcome Measures</h3> Expression of cytokines related to Langerhans cell migration (interleukin [IL] 1, IL-18,and tumor necrosis factor [TNF] α); T_H2 responses(IL-4 and IL-10 ); and T_H1 responses (IL-6, IL-12, and interferon γ). Double staining was performed for elastase (neutrophils), tryptase (mast cells),and CD36 (macrophages). <h3>Results</h3> The number of cells expressing IL-1β and TNF-α was reduced in the UV-B–exposed skin of patients with PLE compared with the skinof healthy individuals (<i>P</i>&lt;.05 for TNF-α). No differences were observed in the expression of T_H1-related cytokinesbut fewer cells expressing IL-4 infiltrated the epidermis of patients withPLE 24 hours after irradiation (<i>P</i>= .03). After UVexposure TNF-α, IL-4, and, to a lesser extent, IL-10 were predominantly expressed by neutrophils. <h3>Conclusions</h3> The reduced expression of TNF-α, IL-4, and IL-10 in the UV-B–irradiated skin of patients with PLE appears largely attributable to a lack of neutrophils,and is indicative of reduced Langerhans cell migration and reduced T_H2 skewing. An impairment of these mechanisms underlying UV-B–induced immunosuppression may be important in the pathogenesis of PLE.