Journal of Prevention and Treatment for Stomatological Diseases ›› 2021, Vol. 29 ›› Issue (12): 859-864.DOI: 10.12016/j.issn.2096-1456.2021.12.010

• Review Articles • Previous Articles    

Research progress on the relationship between IL-37 and periodontitis

ZHENG Xu(),XIE Chen,GAO Chang,GUO Zhuling()   

  1. Department of Stomatology, The First Affiliated Hospital of Hainan Medical University, Haikou 570102, China
  • Received:2020-12-09 Revised:2021-06-15 Online:2021-12-20 Published:2021-08-17
  • Contact: Zhuling GUO
  • Supported by:
    National Natural Science Foundation of China(81660270);Scientific Research Projects of Higher Education in Hainan Province(Hnky2020ZD-19);Hainan Provincial Health Industry Research Project(19A200062)



  1. 海南医学院第一附属医院口腔科,海南 海口(570102)
  • 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:


Periodontitis is the inflammation of periodontal tissue caused by dental plaque, which absorbs the alveolar bone and cementum. The immune response triggered by CD4+T cells is the key factor for the aggravation of periodontitis. The activation of dendritic cells and the receptor activator of the NF-κB ligand (RANKL) pathway is an important link in the alveolar bone resorption of periodontal tissue. Pro-inflammatory factors such as interferon-γ (IFN-γ), tumor necrosis factor (TNF-α) and interleukin-1β (IL-1β) also play important roles in the development of periodontitis. Interleukin-37(IL-37), which is a newly discovered cytokine in the IL-1 family, has five shear variants from a to e, among which the clover β-structure encoded by exon 4 plays an important role in the binding of cytokines and the corresponding receptors. IL-37 has strong anti-inflammatory and inhibition of autoimmunity, can enter the nucleus with the help of caspase-1 and bind with Smad proteins to regulate the transcription of pro-inflammatory genes. Extracellular IL-37 can bind to IL-18 binding protein and inhibit the production of pro-inflammatory factors. IL-37 can inhibit the progression of periodontitis by inhibiting the RANKL signaling pathway, inhibiting the proliferation and differentiation of dendritic cells and CD4+T cells, binding to Smad proteins, and releasing pro-inflammatory factors such as IFN-γ and TNF-α. The IL-37 concentration in periodontal tissue can indicate the progression of periodontitis. Few studies have described the interaction between the anti-inflammatory factor IL-37 and periodontitis. Thus, in this paper, the structure and function of IL-37 and the related factors between IL-37 and periodontitis will be reviewed.

Key words: IL-37, periodontitis, immune response, CD4+T cells, dendritic cells, Smads protein, receptor activator of NF-κB ligand, interferon-γ, tumor necrosis factor-α


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。

关键词: 白细胞介素-37, 牙周炎, 免疫反应, CD4+T细胞, 树突状细胞, Smads蛋白, 核因子-κB受体活化因子配体, 干扰素-γ, 肿瘤坏死因子-α

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