Atopic dermatitis

Atopic dermatitis (AD) is commonly associated with immunoglobulin E (IgE) antibody–related mechanisms, which are the focus of this article. The vast majority of patients with AD exhibit hyperproduction of IgE, particularly during disease onset or flare. IgE-dependent late-phase reactions may influen...

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Bibliographic Details
Published in:Journal of the American Academy of Dermatology 2005-07, Vol.53 (1), p.S86-S93
Main Author: Abramovits, William
Format: Article
Language:English
Subjects:
Adult
Antigen-Presenting Cells - immunology
Child
Comorbidity
Dermatitis, Atopic - epidemiology
Dermatitis, Atopic - genetics
Dermatitis, Atopic - immunology
Dermatitis, Atopic - pathology
Diseases in Twins - epidemiology
Eosinophils - immunology
Humans
Hypersensitivity, Immediate - complications
Hypersensitivity, Immediate - genetics
Immunoglobulin E - immunology
Keratinocytes - immunology
Lymphocyte Subsets - immunology
Macrophages - immunology
Monocytes - immunology
Prevalence
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Summary:Atopic dermatitis (AD) is commonly associated with immunoglobulin E (IgE) antibody–related mechanisms, which are the focus of this article. The vast majority of patients with AD exhibit hyperproduction of IgE, particularly during disease onset or flare. IgE-dependent late-phase reactions may influence the chronic inflammatory response in AD. Clearly, genetics plays a major role in determining who develops AD. However, the recent increase in AD prevalence suggests that a complex interaction between environmental factors and susceptibility genes results in clinical expression of the disorder. These immunologic “triggers” differ among individuals and include various foods, airborne allergens, irritants and contactants, hormones, stress, climate, and microorganisms. Although much about AD remains to be elucidated, our current understanding of its pathophysiology has provided clinicians with the ability to construct more rational therapeutic interventions, including multiple-agent regimens that provide both immediate relief and effective long-term management. Future advances will come from identification of the genes causing this disease and further elucidation of the immunoregulatory mechanisms involved in the pathogenesis of AD.
ISSN:0190-9622
1097-6787
DOI:10.1016/j.jaad.2005.04.034