IL-29 enhances CXCL10 production
Hosokawa, Yoshitaka Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Hosokawa, Ikuko Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Shindo, Satoru Tokushima University
Ozaki, Kazumi Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
oral epithelial cells
Interleukin-29 (IL-29) is a cytokine belonging to the type III interferon family. It was recently detected in the gingival crevicular fluid of periodontitis patients. However, the role of IL-29 in the pathogenesis of periodontal disease remains unknown. The aim of this study was to examine the effects of IL-29 on C-X-C motif chemokine ligand 10 (CXCL10) production in human oral epithelial cells. We measured CXCL10 production in TR146 cells, which is a human oral epithelial cell line, using an enzyme-linked immunosorbent assay. We used Western blot analysis to detect IL-29 receptor expression and the phosphorylation levels of signal transduction molecules, including p38 mitogen-activated protein kinases (MAPK), signal transducer and activator of transcription 3 (STAT3), and nuclear factor (NF)-κB p65, in the TR146 cells. The TR146 cells expressed the IL-29 receptor. IL-29 induced CXCL10 production in the TR146 cells. IL-29 significantly enhanced CXCL10 production in tumor necrosis factor (TNF)-α-stimulated TR146 cells. The p38 MAPK, STAT3, and NF-κB pathways were found to be related to the IL-29-induced enhancement of CXCL10 production in TNF-α-stimulated TR146 cells. IL-29 promotes T helper 1 cell accumulation in periodontal lesions by inducing CXCL10 production in oral epithelial cells.
Immunological Investigations : A Journal of Molecular and Cellular Immunology
Taylor & Francis
This is an Accepted Manuscript of an article published by Taylor & Francis Group in Immunological Investigation on 28/07/2017, available online: http://www.tandfonline.com/10.1080/08820139.2017.1336176.
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