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J Dent Res ; 88(7): 633-8, 2009 Jul.
Article in English | MEDLINE | ID: mdl-19605880

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.


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