Document Detail


The contribution of keratinocytes to the pathogenesis of atopic dermatitis.
MedLine Citation:
PMID:  16581561     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Atopic dermatitis (AD) develops from a complex interplay between environmental, genetic, immunologic and biochemical factors. Relevant to the amplification and persistence of inflammatory and immune responses in AD skin are keratinocytes, which can be induced to secrete proinflammatory mediators in response to a variety of stimuli, including epidermal barrier perturbation. Moreover, keratinocytes from AD patients synthesize exaggerated amounts of mediators (e.g., GM-CSF and RANTES/CCL5) important for enhanced recruitment as well as sustained survival and activation of T cells and dendritic cells. AD keratinocytes have a constitutive dysregulated activity of transcription factors that modulate the expression of inflammatory genes, suggesting the existence of predetermined mechanisms targeting atopic inflammation to the skin. Among these, the existence of a defective epidermal barrier, which appears related to decreased ceramide generation and abnormal degradation of corneodesmosomes, certainly plays a central role in the predisposition to AD.
Authors:
Saveria Pastore; Francesca Mascia; Giampiero Girolomoni
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  European journal of dermatology : EJD     Volume:  16     ISSN:  1167-1122     ISO Abbreviation:  Eur J Dermatol     Publication Date:    2006 Mar-Apr
Date Detail:
Created Date:  2006-04-03     Completed Date:  2006-11-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9206420     Medline TA:  Eur J Dermatol     Country:  France    
Other Details:
Languages:  eng     Pagination:  125-31     Citation Subset:  IM    
Affiliation:
Laboratory of Tissue Engineering and Cutaneous Physiopathology, Istituto Dermopatico dell'Immacolata, IRCCS, via Monti di Creta 104, 00167 Roma, Italy. pastore@idi.it
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MeSH Terms
Descriptor/Qualifier:
Cytokines / biosynthesis
Dermatitis, Atopic / etiology*
Humans
Keratinocytes / physiology*
Chemical
Reg. No./Substance:
0/Cytokines

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