Author(s): Deleuran M, Hvid M, Kemp K, Christensen GB, Deleuran B, , Deleuran M, Hvid M, Kemp K, Christensen GB, Deleuran B,
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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. Copyright © 2012 S. Karger AG, Basel.
This article was published in Chem Immunol Allergy
and referenced in Immunogenetics: Open Access