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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Interleukin-17 regulates the expressions of RANKL and OPG in human periodontal ligament cells via TRAF6/TBK1-JNK/NF-kappa B pathways
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Interleukin-17 regulates the expressions of RANKL and OPG in human periodontal ligament cells via TRAF6/TBK1-JNK/NF-kappa B pathways

机译：白介素17通过TRAF6 / TBK1-JNK /NF-κB通路调节人牙周膜细胞中RANKL和OPG的表达

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摘要

Interleukin-17 (IL-17 or IL-17A), a pleiotropic cytokine produced by T helper type 17 cells, is involved in the pathogenesis of various autoimmune and inflammatory disorders, including periodontitis. Although the ability of pro-inflammation in periodontitis has been widely investigated, the other biological functions of IL-17, including its role in bone remodelling and the underlying molecular mechanisms, have not been well clarified. In the present study, IL-17 could significantly enhance the expression of receptor activator for nuclear factor-kappa B ligand (RANKL) and inhibit the expression of osteoprotegerin (OPG) in human periodontal ligament cells, the two critical indicators for osteoclastogenesis, suggesting that IL-17 may play a destructive role in the pathogenesis of periodontal bone remodelling. Pharmaceutical signal inhibitors targeted at mitogen-activated protein kinases, Akt or nuclear factor-kappa B signals, inhibited IL-17-induced RANKL and OPG regulation. Notably, the enhancement of RANKL was significantly blocked by the inhibitors of c-Jun N-terminal kinase and nuclear factor-kappa B signals. The upstream signals were further investigated with the small interfering RNA. Both tumour necrosis factor receptor-associated factor 6 and TNF receptor associated factor (TRAF) family member-associated nuclear factor kappa-light-chain enhancer of activated B cells (NF-kappa B) activator (TANK)-binding kinase 1 were found to be the critical signal molecules for IL-17-dependent RANKL regulation in human periodontal ligament cells. These findings may provide comprehensive understanding of the role of IL-17 in the pathogenesis of periodontitis and might also provide a reasonable route for periodontitis therapy.
机译：白细胞介素17（IL-17或IL-17A）是由17型T辅助细胞产生的多效性细胞因子，参与各种自身免疫和炎症性疾病（包括牙周炎）的发病机理。尽管已经广泛研究了牙周炎的促炎症反应能力，但尚未充分阐明IL-17的其他生物学功能，包括其在骨重塑中的作用和潜在的分子机制。在本研究中，IL-17可以显着增强核因子-κB配体（RANKL）受体激活剂的表达，并抑制人牙周膜细胞中破骨细胞生成素（OPG）的表达，这是破骨细胞形成的两个关键指标。 IL-17在牙周骨重塑的发病机理中可能发挥破坏作用。靶向有丝分裂原激活的蛋白激酶，Akt或核因子-κB信号的药物信号抑制剂可抑制IL-17诱导的RANKL和OPG调节。值得注意的是，RANKL的增强被c-Jun N-末端激酶和核因子-κB信号的抑制剂显着阻断。用小干扰RNA进一步研究上游信号。发现肿瘤坏死因子受体相关因子6和TNF受体相关因子（TRAF）家族成员相关核因子活化B细胞（NF-κB）激活剂（TANK）结合激酶1的轻链增强子在人牙周膜细胞中是IL-17依赖性RANKL调节的关键信号分子。这些发现可能提供对IL-17在牙周炎发病机制中作用的全面理解，也可能为牙周炎治疗提供合理的途径。

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