title: IL-25 induces both inflammation and skin barrier dysfunction in atopic dermatitis.
abstract: Atopic dermatitis (AD) is a chronic relapsing skin disease characterized by having both an epidermal and a dermal component, shown as a barrier deficiency and inflammation. The mechanisms resulting in skewing the immune response in a Th2 direction in AD are still not fully elucidated. We suggest that IL-25 could be a major target in AD. IL-25 is produced by cells within the dermis of AD patients, and we suggest these to be dendritic cells (DCs). Furthermore, we show that IL-25 can inhibit filaggrin synthesis in keratinocytes. These results point towards a central role of IL-25 producing DCs that can induce both a Th2 response and inhibit filaggrin synthesis. We believe this strongly supports a role for IL-25 in AD, bridging the gap between inflammation and impaired skin barrier function.
authors.forename: Mette
authors.initials: M
authors.lastname: Deleuran
authors.forename: Malene
authors.initials: M
authors.lastname: Hvid
authors.forename: Kaare
authors.initials: K
authors.lastname: Kemp
authors.forename: Gitte B
authors.initials: GB
authors.lastname: Christensen
authors.forename: Bent
authors.initials: B
authors.lastname: Deleuran
authors.forename: Christian
authors.initials: C
authors.lastname: Vestergaard
mesh_terms: D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D000091344:Filaggrin Proteins; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D020381:Interleukin-17 / Q000378:metabolism*; D007381:Intermediate Filament Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D015603:Keratinocytes / Q000378:metabolism; D012867:Skin / Q000503:physiopathology*
chemical_list: C000717249:FLG protein, human; D000091344:Filaggrin Proteins; C486701:IL25 protein, human; D020381:Interleukin-17; D007381:Intermediate Filament Proteins