口腔疾病防治 ›› 2021, Vol. 29 ›› Issue (12): 859-864.DOI: 10.12016/j.issn.2096-1456.2021.12.010
• 综述 • 上一篇
收稿日期:
2020-12-09
修回日期:
2021-06-15
出版日期:
2021-12-20
发布日期:
2021-08-17
通讯作者:
郭竹玲
作者简介:
郑旭,副主任医师,硕士,Email: 基金资助:
ZHENG Xu(),XIE Chen,GAO Chang,GUO Zhuling(
)
Received:
2020-12-09
Revised:
2021-06-15
Online:
2021-12-20
Published:
2021-08-17
Contact:
Zhuling GUO
Supported by:
摘要:
牙周炎为牙菌斑导致的牙周组织炎症,可累及牙骨质、牙周膜及牙槽骨,由CD4+T细胞引发的免疫反应是牙周炎加重的关键因素,树突状细胞及核因子-κB受体活化因子配体(receptor activator of NF-κB ligand,RANKL)途径的激活是牙槽骨吸收的重要环节,促炎因子IFN-γ、TNF-α、IL-1β在牙周炎的发生发展中亦发挥重要作用。白细胞介素-37(interleukin-37,IL-37)为IL-1家族新发现的细胞因子,具有a~e共5个剪切变异体,其中由第4号外显子编码的三叶草β状结构对细胞因子和相应受体的结合具有重要作用。IL-37具有强大的抗炎和抑制自身免疫作用,可在caspase-1酶作用下进出细胞核,在细胞内与Smads蛋白结合调控促炎基因的转录;在细胞外IL-37可与IL-18结合蛋白结合,抑制促炎因子的产生。IL-37可通过抑制树突状细胞、CD4+T细胞的增殖、分化,与Smads蛋白结合、抑制RANKL信号途径及促炎因子如IFN-γ、TNF-α的释放抑制牙周炎的进展,牙周组织IL-37浓度可作为牙周炎进展状态的监测指标。目前,鲜见关于抗炎因子IL-37与牙周炎相互作用的描述,本文对IL-37的结构功能及与牙周炎的关系进行综述。
中图分类号:
郑旭,谢琛,高畅,郭竹玲. 白细胞介素-37与牙周炎关系的研究进展[J]. 口腔疾病防治, 2021, 29(12): 859-864.
ZHENG Xu,XIE Chen,GAO Chang,GUO Zhuling. Research progress on the relationship between IL-37 and periodontitis[J]. Journal of Prevention and Treatment for Stomatological Diseases, 2021, 29(12): 859-864.
图1 IL-37发挥抗炎作用的细胞内、细胞外途径
Figure 1 The anti-inflammatory effects of IL-37 through intracellular and extracellular pathways IL-1R8: interleukin-1 receptor 8; IL-18BP: interleukin-18 binding protein; IL-18Rα: interleukin-18 receptor α; TLR: toll-like receptor; TNF-α: tumor necrosis factor-α; IFN-γ: interferon-γ
图2 IL-37抑制树突状细胞、CD4+T细胞增殖分化
Figure 2 IL-37 inhibits proliferation and differentiation of dendritic cells and CD4+T cells TLR4: toll-like receptor 4; RANKL: receptor activator of NF-κB ligand; Foxp3: forked head transcription factor 3; TGF-β: transforming growth factor-β; IL: interleukin
图3 IL-37通过抑制RANKL途径延缓牙槽骨吸收
Figure 3 IL-37 delays alveolar bone resorption through inhibiting the RANKL pathway RANKL: receptor activator of NF-κB ligand; RANK: receptor activator of NF-κB; IL: interleukin
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