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March 1994

The Immunopathogenesis of Vitiligo

Author Affiliations

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. doi:10.1001/archderm.1994.01690030123022

The recent article by Gilhar and coworkers1 adds to the list of recent works2,3 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

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