IL‐33 induces Egr‐1‐dependent TSLP expression via the MAPK pathways in human keratinocytes

• DOI: 10.1111/exd.12788
• Publication Date: 2015-06-29T10:59:10Z
• Authors: Woo‐In Ryu; Hana Lee; Jin Hee Kim; Hyun Cheol Bae; Hwa Jung Ryu; Sang Wook Son
• Keywords: Keratinocytes; 0303 health sciences; 03 medical and health sciences; Thymic Stromal Lymphopoietin; MAP Kinase Signaling System; Cytokines; Humans; Interleukin-33; Cells, Cultured; Dermatitis, Atopic; Early Growth Response Protein 1

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 an important role AD. IL-33 highly expressed AD, but its AD has not yet fully understood. To further identify the of we investigated expression TSLP induced by keratinocytes. This study revealed that human Early growth response protein 1 (Egr)-1, transcriptional factor, IL-33. IL-33-mediated induction keratinocytes was suppressed treatment with mitogen-activated kinase (MAPK) inhibitors or small interfering RNA against Egr-1. Chromatin immunoprecipitation (ChIP) assay indicated direct involvement Egr-1 induction. Taken together, these findings indicate may increase through Egr-1-dependent mechanism via ERK1/2, JNK p38 activation These data suggest IL-33-ERK/JNK/p38/Egr-1/TSLP axis involved allergic inflammation, it be novel therapeutic target.