title: Skin barrier defects in atopic dermatitis.
abstract: Atopic dermatitis (AD) is a chronic inflammatory skin condition with complex etiology that is dependent upon interactions between the host and the environment. Acute skin lesions exhibit the features of a Th2-driven inflammatory disorder, and many patients are highly atopic. The skin barrier plays key roles in immune surveillance and homeostasis, and in preventing penetration of microbial products and allergens. Defects that compromise the structural integrity or else the immune function of the skin barrier play a pivotal role in the pathogenesis of AD. This article provides an overview of the array of molecular building blocks that are essential to maintaining healthy skin. The basis for structural defects in the skin is discussed in relation to AD, with an emphasis on filaggrin and its genetic underpinnings. Aspects of innate immunity, including the role of antimicrobial peptides and proteases, are also discussed.
authors.affiliation: Department of Medicine, University of Virginia Health System, Allergy Division, PO Box 801355, Charlottesville, VA, 22908-1355, USA, ra8w@virginia.edu.
authors.forename: Rachana
authors.initials: R
authors.lastname: Agrawal
authors.forename: Judith A
authors.initials: JA
authors.lastname: Woodfolk
mesh_terms: D000818:Animals; D003876:Dermatitis, Atopic / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology; D000091344:Filaggrin Proteins; D006801:Humans; D008051:Lipid Bilayers / Q000276:immunology; D010447:Peptide Hydrolases / Q000276:immunology; D011480:Protease Inhibitors / Q000627:therapeutic use; D012867:Skin / Q000276:immunology* / Q000503:physiopathology; D019108:Tight Junctions / Q000276:immunology
chemical_list: C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D008051:Lipid Bilayers; D011480:Protease Inhibitors; D010447:Peptide Hydrolases