TY - JOUR
T1 - The involvement of IL-23 and the Th 17 pathway in periodontitis
AU - Ohyama, H.
AU - Kato-Kogoe, N.
AU - Kuhara, A.
AU - Nishimura, F.
AU - Nakasho, K.
AU - Yamanegi, K.
AU - Yamada, N.
AU - Hata, M.
AU - Yamane, J.
AU - Terada, N.
PY - 2009/7/1
Y1 - 2009/7/1
N2 - 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 β2 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-γ, 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.
AB - 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 β2 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-γ, 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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U2 - 10.1177/0022034509339889
DO - 10.1177/0022034509339889
M3 - Article
C2 - 19605880
AN - SCOPUS:68249143144
SN - 0022-0345
VL - 88
SP - 633
EP - 638
JO - Journal of Dental Research
JF - Journal of Dental Research
IS - 7
ER -