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J Invest Dermatol. 2011 Jan;131(1):150-7. doi: 10.1038/jid.2010.277. Epub 2010 Sep 23.

IL-25 in atopic dermatitis: a possible link between inflammation and skin barrier dysfunction?

Author information

1
Institute of Medical Microbiology and Immunology, Aarhus University, Aarhus C, Denmark. malenel@microbiology.au.dk

Abstract

Atopic dermatitis (AD) is a common skin disease associated with a T(H)2 response and increased levels of T(H)2-associated cytokines and IgE. The mechanisms resulting in skewing the immune response in a T(H)2 direction in AD are not fully elucidated. However, such skewing has recently been associated with IL-25 in a murine model for allergic airway disease. The aim of this study was to investigate whether IL-25 may have a role in AD. We have identified IL-25-producing cells within the dermis of AD patients and propose that these cells are dendritic cells (DCs). This is supported by in vitro experiments that indicate that monocyte-derived DCs are capable of producing IL-25. As null mutations of filaggrin are associated with the development of an impaired skin barrier in AD, we investigated whether IL-25 affects filaggrin synthesis by keratinocytes. Using mRNA analysis, we have shown that IL-25 stimulation does indeed decrease filaggrin synthesis in cultured keratinocytes. These results suggest that IL-25 produced by DCs could have a dual role as both an inducer of the T(H)2 response and as an inhibitor of filaggrin synthesis, thereby directly affecting skin barrier function in AD patients.

PMID:
20861853
DOI:
10.1038/jid.2010.277
[Indexed for MEDLINE]
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