期刊
JOURNAL OF DENTAL RESEARCH
卷 88, 期 7, 页码 633-638出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0022034509339889
关键词
periodontitis; interleukin (IL)-23; Th17; IL-12; cellular immune response
资金
- Japan Society for the Promotion of Science [18592274, 19592399]
- Grants-in-Aid for Scientific Research [18592274, 19592399] Funding Source: KAKEN
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 beta 2 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.
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