Atopic dermatitis - 21/08/11
Dallas, Texas
Résumé |
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.
Le texte complet de cet article est disponible en PDF.Abbreviations used : AD, APC, ECP, FcεRI, GM-CSF, IDEC, IFN-⍺ -β, -γ, IgE, IL-1 -2, etc, LC, mRNA, PDC, SC, TH0, TH1, TH2, TNF
Plan
This article is part of a supplement supported by Connetics Corp, Palo Alto, California. Disclosure: Dr Abramovits has received research support and/or is a consultant and lecturer for Fujisawa Healthcare, Novartis Pharmaceuticals Corp, Ferndale Laboratories, Abbott Laboratories, Connetics Corp, Amgen, Biogen Idec, Centocor, Genentech, and Galderma. |
Vol 53 - N° 1S
P. S86-S93 - juillet 2005 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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