IL-29 Enhances CXCL10 Production in TNF-α-stimulated Human Oral Epithelial Cells

  • Yoshitaka Hosokawa
  • , Ikuko Hosokawa
  • , Satoru Shindo
  • , Kazumi Ozaki
  • , Takashi Matsuo

Research output: Contribution to journalArticlepeer-review

Abstract

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 a 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.

Original languageEnglish
Pages (from-to)615-624
Number of pages10
JournalImmunological Investigations
Volume46
Issue number6
DOIs
StatePublished - Aug 18 2017
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2017 Taylor & Francis.

ASJC Scopus Subject Areas

  • Immunology

Keywords

  • CXCL10
  • IL-29
  • oral epithelial cells

Fingerprint

Dive into the research topics of 'IL-29 Enhances CXCL10 Production in TNF-α-stimulated Human Oral Epithelial Cells'. Together they form a unique fingerprint.

Cite this