Skin barrier function.
Like other inflammatory dermatoses, the pathogenesis of atopic dermatitis (AD) has been largely attributed to abnormalities in adaptive immunity. T helper (Th) cell types 1 and 2 cell dysregulation, IgE production, mast cell hyperactivity, and dendritic cell signaling are thought to account for the chronic, pruritic, and inflammatory dermatosis that characterizes AD. Not surprisingly, therapy has been directed toward ameliorating Th2-mediated inflammation and pruritus. Here, we review emerging evidence that inflammation in AD occurs downstream to inherited and acquired insults to the barrier. Therapy based upon this new view of pathogenesis should emphasize approaches that correct the primary abnormality in barrier function, which drives downstream inflammation and allows unrestricted antigen access.
Elias
Peter M
PM
Dermatology Service (190), VA Medical Center, 4150 Clement Street, San Francisco, CA 94121, USA. eliasp@derm.ucsf.edu
D000818:Animals; D003876:Dermatitis, Atopic / Q000235:genetics / Q000276:immunology / Q000503:physiopathology* / Q000628:therapy*; D000091344:Filaggrin Proteins; D006801:Humans; D007381:Intermediate Filament Proteins / Q000378:metabolism; D012867:Skin / Q000276:immunology / Q000378:metabolism / Q000382:microbiology / Q000503:physiopathology*
D000091344:Filaggrin Proteins; D007381:Intermediate Filament Proteins