Document Detail


Evolving concepts of pathogenesis in atopic dermatitis and other eczemas.
MedLine Citation:
PMID:  18719604     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The eczemas represent a common and diverse group of inflammatory skin diseases whose definitions and pathogenic mechanisms have often been confused and controversial. Since the millennium, fresh approaches are providing better insight. Research has focused much more upon the epidermis and the very relevant signaling pathways that contribute to spongiosis, proliferation, generation of proinflammatory factors, and differentiation to form an effective stratum corneum barrier. A major step in understanding has come from the solidly confirmed association between filaggrin null mutations of ichthyosis vulgaris and atopic dermatitis. Similar associations relating to protease and lipid defects have highlighted the role of barrier disruption that allows greater access of environmental toxins, microbes, and allergens. Animal models are beginning to predict mechanisms in which such direct perturbation of keratinocytes may initiate inflammation and condition immune responses in irritant contact dermatitis and atopic dermatitis. These conceptual shifts are nurturing more balanced approaches to understanding eczema and hold the hope for better prevention efforts and more specific molecular targeting for therapy.
Authors:
Jon M Hanifin
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Publication Detail:
Type:  Journal Article; Review     Date:  2008-08-21
Journal Detail:
Title:  The Journal of investigative dermatology     Volume:  129     ISSN:  1523-1747     ISO Abbreviation:  J. Invest. Dermatol.     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-01-16     Completed Date:  2009-02-27     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0426720     Medline TA:  J Invest Dermatol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  320-2     Citation Subset:  IM    
Affiliation:
Department of Dermatology, Oregon Health & Science University, 3303 S.W. Bond Avenue, Portland, OR 97239-4501, USA. hanifinj@ohsu.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Dermatitis, Atopic / etiology*,  immunology*
Eczema / etiology*,  immunology*
Humans
Keratinocytes / immunology*
Signal Transduction / immunology

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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