| Literature DB >> 30484005 |
Satoru Shindo1, Yoshitaka Hosokawa2, Ikuko Hosokawa2, Hideki Shiba3.
Abstract
Interleukin (IL)-35 is a novel anti-inflammatory cytokine that is produced by regulatory T cells. IL-35 is reported to suppress IL-17A-producing helper T (Th17) cell activation. IL-17A is related to progression of periodontitis. Furthermore, IL-35 and IL-17A are detected in human gingival crevicular fluid. However, the effect of IL-35 and interaction between IL-35 and IL-17A on pro-inflammatory cytokine production in human periodontal resident cells are still unclear. The aim of this study was to clarify the effect of IL-35 on IL-6 and IL-8 production in human periodontal ligament cells (HPDLCs) stimulated with IL-17A. IL-35 inhibited IL-6 and IL-8 production in IL-17A-stimulated HPDLCs. Moreover, western blot analysis showed that IL-35 suppressed extracellular signal-regulated kinase (ERK) and nuclear factor (NF)-κB p65 phosphorylation in IL-17A-stimulated HPDLCs. Our findings suggested that IL-35 produced from regulatory T cells might inhibit progression of periodontitis by decreasing IL-17A-induced levels of IL-6 and IL-8.Entities:
Keywords: IL-17A; IL-35; IL-6; IL-8; human periodontal ligament cells
Year: 2019 PMID: 30484005 DOI: 10.1007/s10753-018-0938-9
Source DB: PubMed Journal: Inflammation ISSN: 0360-3997 Impact factor: 4.092