The involvement of IL-23 and the Th17 pathway in periodontitis

J Dent Res. 2009 Jul;88(7):633-8. doi: 10.1177/0022034509339889. Epub 2009 Jul 15.

Abstract

Interleukin (IL)-23 is an essential cytokine involved in expansion of the Th17 lineage, which is associated with many immune-related destructive tissue diseases. We hypothesized that the IL-23-induced Th17 pathway plays a role in periodontal pathology and examined the expression of cytokines, and related molecules, in periodontal lesions and control sites. IL-23 and IL-12 were expressed at significantly higher levels in periodontal lesions than in control sites. However, the relative expression of the IL-23 receptor compared with the IL-12 receptor beta2 was significantly higher in periodontal lesions. Moreover, IL-17 expression was significantly higher in periodontal lesions, especially in the tissue adjacent to bone destruction, than in control sites. There was no significant difference in the expression levels of IFN-gamma, an important cytokine inhibiting differentiation toward the Th17 pathway, between periodontal lesions and control sites. Together, these results suggest that the IL-23-induced Th17 pathway is stimulated in inflammatory periodontal lesions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD4-Positive T-Lymphocytes / metabolism*
  • Case-Control Studies
  • Chronic Periodontitis / immunology*
  • Chronic Periodontitis / metabolism*
  • Female
  • Gene Expression
  • Humans
  • Immunohistochemistry
  • Interferon-gamma / biosynthesis
  • Interleukin-12 / biosynthesis
  • Interleukin-17 / biosynthesis*
  • Interleukin-23 / biosynthesis*
  • Male
  • Middle Aged
  • Polymerase Chain Reaction
  • Receptors, Interleukin / biosynthesis
  • Receptors, Interleukin-12 / biosynthesis

Substances

  • IL23R protein, human
  • Interleukin-17
  • Interleukin-23
  • Receptors, Interleukin
  • Receptors, Interleukin-12
  • Interleukin-12
  • Interferon-gamma