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| Research article summary (published 30 Jul 2001): |
Immunohistology of drug-induced exanthema: clues to pathogenesis.
Full Abstract
Hypersensitivity reactions to drugs can cause a variety of different skin disorders, the most frequent being maculopapular eruptions. In recent years increasing evidence has indicated the important involvement of T cells in this drug reaction. Histopathological changes typically show a dominant T-cell infiltration together with vacuolar interface dermatitis. Immunohistochemical studies demonstrate the presence of cytotoxic CD4+ and CD8+ T cells, which contain perforin and granzyme B, in close proximity to keratinocytes showing signs of cell destruction. Expression of Fas ligand is barely detectable, which suggests that cytotoxic granule exocytosis may be the dominant pathway leading to keratinocyte cell damage. In addition, drug-specific T cells may orchestrate the inflammatory skin reaction through the release and induction of various cytokines (i.e. IL-5, IL-6, TNF-alpha, IFN-gamma) and chemokines (i.e. regulated on activation, normal T-cell expressed and secreted; eotaxin). These mediators contribute to the generation of eosinophilia, which may amplify the underlying immune response through the release of further proinflammatory mediators in drug-induced maculopapular exanthema.
Author information
Author/s: Yawalkar, N (N); Pichler, W J (WJ);
Affiliation: Harvard Skin Disease Research Center, Harvard Institutes of Medicine, Boston, Massachusetts 02115, USA. nyawalkar(-atsign-)rics.bwh.harvard.edu
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Review
Journal: Current opinion in allergy and clinical immunology (Curr Opin Allergy Clin Immunol), published in United States. (Language: eng)
Reference: 2001-Aug; vol 1 (issue 4) : pp 299-303
Dates: Created 2002/04/19; Completed 2002/06/13; Revised 2006/11/15;
PMID: 11964704, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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