国际口腔医学杂志 ›› 2025, Vol. 52 ›› Issue (4): 514-525.doi: 10.7518/gjkq.2025058

• 综述 • 上一篇    下一篇

辅助性T细胞17与调节性T细胞之间的制衡效应调控口腔颌面部骨损伤修复的研究进展

祝舒钰1(),周静2,谢志刚1()   

  1. 1.昆明医科大学附属口腔医院种植科 昆明 650106
    2.昆明医科大学附属延安医院口腔科 昆明 650051
  • 收稿日期:2024-09-10 修回日期:2025-02-11 出版日期:2025-07-01 发布日期:2025-06-20
  • 通讯作者: 谢志刚
  • 作者简介:祝舒钰,住院医师,硕士,Email:2394105393@qq.com
  • 基金资助:
    兴滇英才-医疗卫生人才项目(XDYC-YLWS-2023-049);云南省科技厅昆明医科大学联合专项重点项目(202101AY070001-025);云南省口腔疾病临床医学研究中心重点项目(2022ZD005)

Balance between T-helper 17 cells and regulatory T cells in bone remodeling and their impact on oral and maxillofacial damage recovery

Shuyu Zhu1(),Jing Zhou2,Zhigang Xie1()   

  1. 1.Dept. of Oral Implantology, the Affiliated Stomatology Hospital of Kunming Medical University, Kunming 650106, China
    2.Dept. of Stomatology, Yan’an Hospital, Kunming Medical University, Kunming 650051, China
  • Received:2024-09-10 Revised:2025-02-11 Online:2025-07-01 Published:2025-06-20
  • Contact: Zhigang Xie
  • Supported by:
    Xingdian Talents-Medical and Health Care Talent Project(XDYC-YLWS-2023-049);Key Joint Special Project of Yunnan Provincial Science and Technology Department and Kunming Medical University(202101AY070001-025);Key Project of Yunnan Clinical Research Center for Oral Diseases(2022ZD005)

摘要:

骨损伤后的骨组织重塑直至最终修复,是一个受到严格调控的动态过程。其中,免疫系统的调控作用日益受到研究者们的重视。在诸多免疫细胞中,辅助性T细胞17(Th17)和调节性T细胞(Treg)分别以促炎和抑炎效应对骨代谢相关细胞的功能与活性发挥着重要的调控作用,Th17/Treg细胞平衡失调与多种骨代谢疾病密切相关,调节这一平衡可能为骨损伤修复提供新的策略。本文旨在对Th17与Treg细胞在骨重塑中的制衡调节机制,以及干预Th17/Treg细胞平衡以促进口腔颌面部骨损伤修复的研究现状作一综述。

关键词: 辅助性T细胞17, 调节性T细胞, 细胞平衡, 骨免疫, 牙周炎, 种植体周围炎

Abstract:

Bone tissue remodeling during bone injury recovery is a well-regulated dynamic process, of which the pro-minent role of immune balance on bone homeostasis is increasingly understood. Among the various immune cells, T-hel-per 17 cells (Th17) and regulatory T cells (Treg) have attracted considerable attention because of their contradictive roles in inflammatory response and bone homeostasis. The imbalance of the Th17/Treg cell balance is closely associated with va-rious bone metabolism disorders, and regulating this balance may provide novel strategies for bone injury repair. Thus, this review focuses on the balance between Th17 and Treg in bone remodeling and their impacts on oral and maxillofacial damage recovery.

Key words: T-helper 17 cell, regulatory T cell, cell balance, osteoimmunology, periodontitis, peri-implantitis

中图分类号: 

  • R782.2

表 1

Th17在骨免疫中的作用及相关机制"

细胞功能细胞因子目标机制参考文献
Th17↑骨吸收↑IL-17↑破骨细胞调节破骨细胞的能量代谢[60]
涉及 IL-17/RANKL/TRAF6信号通路[58]
增加RANKL/OPG比例以上调破骨细胞数量及大小[57]
上调RANK并增加破骨细胞前体细胞对RANKL刺激的敏感性[56]
↓成骨细胞涉及IL-23-IL-17信号轴[47]
减少分泌ALP、OCN、Osx[68]
↑TNF-α↑破骨细胞通过RANKL促进破骨[70]
↑巨噬细胞通过NF-κB和SAPK/JNK信号通路增加巨噬细胞RANKL的表达[71]
↑B细胞诱导B细胞产生RANKL刺激破骨细胞生成,进而引发骨丢失[72]
↓成骨细胞增强Wnt信号通路抑制剂DKK1的表达[73-74]
通过增加P2Y2受体表达促进成骨细胞凋亡[75]
Th17↑ 骨生成↑IL-17↑成骨细胞、间充质干细胞促进间充质干细胞由成脂向转化为成软骨向分化[61-63]
促成骨作用可被ROS清除剂或Act1的敲除所抑制[57]
通过p-STAT3与NRF2相互作用抑制成骨细胞铁死亡[67]
促进矿化结节的形成,并增加Runx2的表达[66]

表 2

Treg在骨免疫中的作用及相关机制"

细胞功能细胞因子/直接接触目标机制参考文献
Treg↓骨吸收↑IL-10↓破骨细胞上调OPG并下调RANKL和M-CSF以抑制破骨细胞的分化和成熟[78]
↓巨噬细胞抑制巨噬细胞向破骨细胞的分化[77]
↑TGF-β1↓破骨细胞通过Smad、MAPK和Bcl2途径诱导破骨细胞凋亡[81]
CTLA4↓破骨细胞前体细胞与CD80/CD86结合以促进破骨细胞前体细胞凋亡[41,80]
Treg↑ 骨生成↑TGF-β1↑成骨细胞、间充质干细胞涉及PI3K/AKT/mTOR/S6激酶1信号通路[93]
激活细胞内效应物,如MAPK和Smad相关蛋白[90,92]
Tregs促进NFAT1-SMAD3复合物在CD8+T细胞中合成,进一步驱动Wnt10b的表达[95]
发挥软骨诱导作用,抑制软骨吸收[96]
Treg↑ 骨吸收↑TGF-β1↑破骨细胞阻断Smad3与TRAF6-TAB1-TAK1复合物的结合[83]
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