白细胞介素⁃37与牙周炎关系的研究进展  

Research progress on the relationship between IL⁃37 and periodontitis

作　　者：郑旭[1] 谢琛 高畅 郭竹玲 ZHENG Xu;XIE Chen;GAO Chang;GUO Zhuling(Department of Stomatology,The First Affiliated Hospital of Hainan Medical University,Haikou 570102,China)

机构地区：[1]海南医学院第一附属医院口腔科,海南海口570102

出　　处：《口腔疾病防治》2021年第12期859-864,共6页Journal of Prevention and Treatment for Stomatological Diseases

基　　金：国家自然科学基金项目(81660270);海南省高等学校科学研究重点项目(Hnky2020ZD⁃19);海南省卫生健康行业科研项目(19A200062)。

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 activatorofNF⁃κB li⁃gand,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。Periodontitis is the inflammation of periodontal tissue caused by dental plaque,which absorbs the alveo⁃lar bone and cementum.The immune response triggered by CD4^(+)T cells is the key factor for the aggravation of periodon⁃titis.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.Inter⁃leukin⁃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 cloverβ⁃structure encoded by exon 4 plays an important role in the binding of cytokines and the correspond⁃ing 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⁃γand 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.

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 

分 类 号：R78[医药卫生—口腔医学]