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

Abstract:

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