Department of Stomatology, Shengjing Hospital of China Medical University, San Hao St. No. 36, Shenyang, 110004, Liaoning, China.
Inflammation. 2018 Oct;41(5):1791-1803. doi: 10.1007/s10753-018-0822-7.
Periodontitis is a dysbiotic bacteria-mediated disease characterized by periodontal inflammations and alveolar bone damage. Its mechanisms were complicated, involving an inflammation-mediated bone destruction. We sought to determine roles and rules that CD8 regulatory T cells (CD8 Tregs) affect alveolar bone homeostasis during periodontitis. Presence of CD8 Tregs in the gingiva, cervical lymph nodes (CLNs), and spleens of healthy or periodontitis animals was analyzed. CD8 regulatory T cells from periodontitis animals were sorted by magnetic-activated cell sorting and fluorescent-activated cell sorting technique, subsequently injected into recipient animals to set adoptive transfer model. We induced experimental periodontitis on transfer models and equal number healthy animals. Four weeks later, their alveolar bone loss and osteoclast coverage length were measured. We also detected CD8 Tregs, CD4 T cell, CD4 Tregs, Th17 cell, and IL-1β, IL-6, IL-10, IL-17A, RANKL, TGF-β expression in the gingiva, CLNs, and spleen to illustrate possible working mechanism of CD8 regulatory T cells. Periodontitis does not induce significant change on proportion or amount of CD8 Tregs. Adoptive transfer of CD8 Tregs reduces alveolar bone destruction and osteoclast formation. In addition, experimental periodontitis increases percentage of Th17 cells and decreases CD4 Tregs in the gingiva and CLNs. More IL-1β, IL-6, IL-17A, and RANKL, and less IL-10 and TGF-β are also detected in the gingiva and CLNs from animals with periodontitis than the one from healthy animals. Adoptive transfer of CD8 regulatory T cells remedies all above pathological change effectively. We did not find any significant difference in spleen, regardless group and detected items. Outcomes of present study clarify function that CD8 regulatory T cells affect alveolar bone homeostasis, and disclose its possible working mechanisms. CD8 regulatory T cells protect alveolar bone via reducing osteoclastogenesis and modulating local immune response.
牙周炎是一种由细菌失调引起的疾病,其特征是牙周炎症和牙槽骨破坏。其机制复杂,涉及炎症介导的骨破坏。我们试图确定 CD8 调节性 T 细胞(CD8 Tregs)在牙周炎期间影响牙槽骨动态平衡的作用和规律。分析健康或牙周炎动物牙龈、颈部淋巴结(CLN)和脾脏中 CD8 Tregs 的存在情况。通过磁激活细胞分选和荧光激活细胞分选技术对来自牙周炎动物的 CD8 调节性 T 细胞进行分选,然后将其注入受者动物中建立过继转移模型。我们在转移模型和等量的健康动物上诱导实验性牙周炎。四周后,测量其牙槽骨丢失和破骨细胞覆盖长度。我们还检测了牙龈、CLN 和脾脏中的 CD8 Tregs、CD4 T 细胞、CD4 Tregs、Th17 细胞和 IL-1β、IL-6、IL-10、IL-17A、RANKL、TGF-β 的表达,以说明 CD8 调节性 T 细胞的可能作用机制。牙周炎不会引起 CD8 Tregs 比例或数量的显著变化。CD8 Tregs 的过继转移可减少牙槽骨破坏和破骨细胞形成。此外,实验性牙周炎增加了牙龈和 CLN 中 Th17 细胞的比例,降低了 CD4 Tregs 的比例。牙周炎动物牙龈和 CLN 中还检测到更多的 IL-1β、IL-6、IL-17A 和 RANKL,以及更少的 IL-10 和 TGF-β。与健康动物相比。过继转移 CD8 调节性 T 细胞可有效纠正所有上述病理变化。无论组和检测项目如何,在脾脏中均未发现任何显著差异。本研究的结果阐明了 CD8 调节性 T 细胞影响牙槽骨动态平衡的功能,并揭示了其可能的作用机制。CD8 调节性 T 细胞通过减少破骨细胞生成和调节局部免疫反应来保护牙槽骨。