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NLRP3炎症小体在自身免疫性肝炎中的作用机制
DOI: 10.12449/JCH241027
利益冲突声明：本文不存在任何利益冲突。
作者贡献声明：王丽菲、罗龙龙负责检索文献，撰写论文；邢国静、卢利霞、李斌参与修改论文；于晓辉、张久聪负责拟定写作思路，指导撰写文章并最后定稿。
Research advances in the mechanism of action of nucleotide-binding oligomerization domain-like receptor protein 3 inflammasome in autoimmune hepatitis
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摘要: 自身免疫性肝炎（AIH）是由自身免疫系统攻击肝细胞所致的慢性肝炎，目前关于AIH的发病机制尚不十分明确。炎症小体是先天免疫的重要组成部分，参与多种病理生理学过程。研究表明核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）炎性小体相关的炎性反应在AIH的发病机制中起重要作用，其主要介导促炎因子的释放和细胞焦亡，进而参与AIH的病理生理过程。因此，可以通过抑制NLRP3炎性小体的激活来延缓AIH发生发展，从而为AIH的防治提供新思路。
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关键词:
- 肝炎， 自身免疫性 /
- NLR家族，热蛋白结构域包含蛋白3 /
- 治疗学
Abstract: Autoimmune hepatitis （AIH） is chronic hepatitis caused by the attack of live cells by the immune system， and at present， the pathogenesis of AIH remains unclear. Inflammasomes are important components of innate immunity and are involved in a variety of pathophysiological processes. Studies have shown that inflammatory response associated with nucleotide-binding oligomerization domain-like receptor protein 3 （NLRP3） plays an important role in the pathogenesis of AIH， which mainly mediates the release of proinflammatory factors and pyroptosis， thereby participating in the pathophysiological process of AIH. Therefore， the development and progression of AIH can be delayed by inhibiting the activation of NLRP3 inflammasomes， which provides new ideas for the prevention and treatment of AIH. -
图 1 NLRP3炎症小体激活机制
注： TLR，Toll样受体；pro-IL-1β，前体IL-1β；pro-IL-18，前体IL-18；NEK7，NIMA相关激酶7；LRR，富亮氨酸重复序列；P2X7R，嘌呤能2X7受体；ROS，活性氧。
Figure 1. Mechanism of NLRP3 inflammatory activation
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