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Arch Dermatol. 2004;140:351-352.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Polymorphic light eruption (PLE) is possibly the most common chronic skin disorder in people living in temperate climes. Self-report questionnaire surveys suggest a prevalence of about 15% in the northern hemisphere.¹ It is therefore appropriate that the current research programs of some specialist centers include a reassessment of this disease, including its cause and diagnosis.

In this issue of the ARCHIVES, 2 articles address different aspects of PLE. A team of Dutch investigators² have examined the mechanism of the apparent underlying immune defect, whereas a British group³ reassessed the methodology of provocation of the disorder.

In an earlier article, Kölgen et al⁴ reported that UV-induced Langerhans cell (LC) migration from the skin was impaired in PLE patients. It was therefore postulated that the pathologic defect underlying PLE might be a failure of normal photoimmunosuppression. Thus the balance of UV-induced suppression and UV-induced provocation would be altered, allowing sunlight exposure to . . . [Full Text of this Article]

Lesley E. Rhodes, MD, FRCP
Photobiology Unit, Dermatology Centre
Clinical Sciences Building
University of Manchester Hope Hospital
Salford M6 8HD, England
(e-mail: lesley.e.rhodes@man.ac.uk)

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