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Correlation With Langerhans Cell Migration and Immunosuppression

Wendy Kölgen, MSc; Marjan van Meurs, BSc; Marjan Jongsma, BSc; Huib van Weelden, MSc; Carla A. F. M. Bruijnzeel-Koomen, MD; Edward F. Knol, PhD; Willem A. van Vloten, MD; Jon Laman, PhD; Frank R. de Gruijl, PhD

Arch Dermatol. 2004;140:295-302.

Background  Disturbances in UV-induced Langerhans cell migration and T helper (T_H) 2 cell responses could be early steps in the pathogenesis of PLE.

Objective  To establish whether UV-B exposure induces aberrant cytokine expression in the uninvolved skin of patients with polymorphous light eruption (PLE).

Design  Immunohistochemical staining and comparison of microscopic sections of skin irradiated with 6 times the minimal dose of UV-B causing erythema and the unirradiated skin of patients with PLE and of healthy individuals.

Setting  University Medical Center (Dutch National Center for Photodermatoses).

Patients  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.

Main Outcome Measures  Expression of cytokines related to Langerhans cell migration (interleukin [IL] 1, IL-18,and tumor necrosis factor [TNF] ); T_H2 responses (IL-4 and IL-10); and T_H1 responses (IL-6, IL-12, and interferon ). Double staining was performed for elastase (neutrophils), tryptase (mast cells), and CD36 (macrophages).

Results  The number of cells expressing IL-1 and TNF- was reduced in the UV-B–exposed skin of patients with PLE compared with the skin of healthy individuals (P<.05 for TNF-). No differences were observed in the expression of T_H1-related cytokines but fewer cells expressing IL-4 infiltrated the epidermis of patients with PLE 24 hours after irradiation (P = .03). After UV exposure TNF-, IL-4, and, to a lesser extent, IL-10 were predominantly expressed by neutrophils.

Conclusions  The reduced expression of TNF-, 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.

From the Department of Dermatology, University Medical Center Utrecht, Utrecht (Ms Kölgen, Mr van Weelden, and Drs Bruijnzeel-Koomen, Knol, and van Vloten); Department of Immunology, Erasmus Medical Center, Rotterdam (Ms van Meurs and Dr Laman); and Department of Dermatology, Leiden University Medical Center, Leiden (Ms Jongsma and Dr de Gruijl), the Netherlands. The authors have no relevant financial interest in this article.

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