Journal
EXPERIMENTAL DERMATOLOGY
Volume 24, Issue 11, Pages 857-863Publisher
WILEY
DOI: 10.1111/exd.12788
Keywords
atopic dermatitis; early growth response protein 1; interleukin-33; mitogen-activated protein kinase; thymic stromal lymphopoietin
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Funding
- Korea Ministry of Environment as a 'Converging technology project'
- Basic Science Research Program through National Research Foundation of Korea (NRF) - Ministry of Science, ICT and Future Planning [NRF-2013R1A2A2A01068137]
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Atopic dermatitis (AD) is a chronic inflammatory skin disease in which T-helper type 2 (Th2)-type immune responses are dominant. Th2 cytokine, interleukin (IL)-33 and thymic stromal lymphopoietin (TSLP) have been suggested to have an important role in AD. IL-33 is highly expressed in AD, but its role in AD has not yet been fully understood. To further identify the role of IL-33 in AD, we investigated the expression of TSLP induced by IL-33 in keratinocytes. This study revealed that IL-33 induced TSLP expression in human keratinocytes. Early growth response protein 1 (Egr)-1, which is an inflammatory transcriptional factor, is induced by IL-33. IL-33-mediated TSLP induction in keratinocytes was suppressed by treatment with mitogen-activated protein kinase (MAPK) inhibitors or small interfering RNA against Egr-1. Chromatin immunoprecipitation (ChIP) assay indicated the direct involvement of Egr-1 in IL-33-mediated TSLP induction. Taken together, these findings indicate that IL-33 may increase TSLP expression through an Egr-1-dependent mechanism via ERK1/2, JNK and p38 activation in keratinocytes. These data suggest that the IL-33-ERK/JNK/p38/Egr-1/TSLP axis is involved in allergic skin Th2 inflammation, and it may be a novel therapeutic target.
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