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B. Torres-Alvarez, MD; B. Moncada, MD; C. Fuentes-Ahumada, Biol; R. Gonzalez-Amaro, MD; L. Baranda, MD
Department of Dermatology and Immunology School of Medicine University of San Luis Potosi Av V Carranza 2405 San Luis Potosi, SLP 78210, Mexico

Arch Dermatol. 1994;130(3):387-388.

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The recent article by Gilhar and coworkers¹ adds to the list of recent works^2,3 that intend to unravel the immunopathogenesis of vitiligo. These articles show that vitiliginous skin responds to the administration of interferon gamma by expressing ICAM-1 in epidermal keratinocytes, a response that occurs in normal skin. The presence of ICAM-1 in keratinocytes appears to be a hallmark of diseases in which there is a hyperimmune status regarding T-cell function, such as in lichen planus. On the other hand, epidermal keratinocytes are incapable of expressing ICAM-1 in diseases characterized by a deficient T-cell response, such as in lepromatous leprosy.^3,4 In 10 biopsy specimens of abnormal and normal contralateral skin taken from patients suffering from generalized vitiligo, we did not find ICAM-1 expression on epidermal keratinocytes when histologic and immunohistochemical staining was performed. For this purpose, antibodies to lymphocyte function— associated antigen (LFA) 1, LFA-2, ICAM-1, and . . . [Full Text PDF of this Article]

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