Document Detail

Cellular and molecular mechanisms in atopic dermatitis.
MedLine Citation:
PMID:  19477321     Owner:  NLM     Status:  MEDLINE    
Atopic dermatitis (AD) is a pruritic inflammatory skin disease associated with a personal or family history of allergy. The prevalence of AD is on the rise and estimated at approximately 17% in the USA. The fundamental lesion in AD is a defective skin barrier that results in dry itchy skin, and is aggravated by mechanical injury inflicted by scratching. This allows entry of antigens via the skin and creates a milieu that shapes the immune response to these antigens. This review discusses recent advances in our understanding of the abnormal skin barrier in AD, namely abnormalities in epidermal structural proteins, such as filaggrin, mutated in approximately 15% of patients with AD, epidermal lipids, and epidermal proteases and protease inhibitors. The review also dissects, based on information from mouse models of AD, the contributions of the innate and adaptive immune system to the pathogenesis of AD, including the effect of mechanical skin injury on the polarization of skin dendritic cells, mediated by keratinocyte-derived cytokines such as thymic stromal lymphopoietin (TSLP), IL-6, and IL-1, that results in a Th2-dominated immune response with a Th17 component in acute AD skin lesions and the progressive conversion to a Th1-dominated response in chronic AD skin lesions. Finally, we discuss the mechanisms of susceptibility of AD skin lesions to microbial infections and the role of microbial products in exacerbating skin inflammation in AD. Based on this information, we discuss current and future therapy of this common disease.
Michiko K Oyoshi; Rui He; Lalit Kumar; Juhan Yoon; Raif S Geha
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Advances in immunology     Volume:  102     ISSN:  0065-2776     ISO Abbreviation:  Adv. Immunol.     Publication Date:  2009  
Date Detail:
Created Date:  2009-05-29     Completed Date:  2009-07-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370425     Medline TA:  Adv Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  135-226     Citation Subset:  IM    
Division of Immunology, Children's Hospital and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.
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MeSH Terms
Dermatitis, Atopic / etiology*,  genetics,  immunology,  physiopathology
Disease Models, Animal
Immunity, Innate
Skin / immunology,  metabolism
Grant Support

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