Abnormal skin barrier in the etiopathogenesis of atopic dermatitis.
Prior studies revealed the key roles played by T-helper type 1 and type 2 (Th1/Th2) cell dysregulation, IgE production, mast cell hyperactivity, and dendritic cell signaling in the evolution of the chronic, pruritic, inflammatory dermatosis that characterizes atopic dermatitis (AD). Accordingly, current therapy has been largely directed toward ameliorating Th2-mediated inflammation and pruritus. This article reviews emerging evidence that the inflammation in AD results from inherited and acquired insults to the barrier, as well as the therapeutic implications of this new paradigm.
Elias
Peter M
PM
Dermatology Service (190), VA Medical Center, San Francisco, CA 94121, USA. eliasp@derm.ucsf.edu
Schmuth
Matthias
M
D001419:Bacteria / Q000276:immunology; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000209:etiology* / Q000276:immunology* / Q000382:microbiology / Q000628:therapy; D000091344:Filaggrin Proteins; D006801:Humans; D007381:Intermediate Filament Proteins / Q000276:immunology*; D012867:Skin / Q000276:immunology* / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology* / Q000378:metabolism*
D016207:Cytokines; D000091344:Filaggrin Proteins; D007381:Intermediate Filament Proteins