自身免疫性肝炎发病机制的研究进展

doi:10.16352/j.issn.1001-6325.2026.08.1135

基础医学与临床 ›› 2026, Vol. 46 ›› Issue (8): 1135-1138.doi: 10.16352/j.issn.1001-6325.2026.08.1135

自身免疫性肝炎发病机制的研究进展

王倩辰^1,2, 万鹏^1,2, 任鑫瑶^1,2, 王阳阳^1*

1.河北大学附属医院消化内科,河北保定 071000;
2.河北大学临床医学院内科学系,河北保定 071000

收稿日期:2025-06-30 修回日期:2025-10-30 发布日期:2026-07-22
通讯作者: ^*wangyangyang2019@126.com

The progress on the pathogenesis of autoimmune hepatitis

WANG Qianchen^1,2, WAN Peng^1,2, REN Xinyao^1,2, WANG Yangyang^1*

1. Department of Gastroenterology, Affiliated Hospital of Hebei University, Baoding 071000;
2. Department of Internal Medicine, Clinical Medical College of Hebei University, Baoding 071000, China

Received:2025-06-30 Revised:2025-10-30 Published:2026-07-22
Contact: ^*wangyangyang2019@126.com

摘要/Abstract

摘要： 自身免疫性肝炎(AIH)是一种由免疫介导的慢性肝脏炎性反应。由于免疫系统对肝脏自身抗原的识别障碍,多种免疫细胞发生激活,继而释放了大量的炎性因子。自身抗原与炎性因子作用于细胞表面的受体,激活了NF-κB、AMPK、PI3K/Akt、JAK/STAT和MAPK等多个信号通路,通过调节树突状细胞、巨噬细胞、T细胞等免疫细胞的能量代谢、细胞自噬、细胞凋亡和受体的表达等多种方式诱发或加重肝脏的免疫性损伤。

关键词: 自身免疫性肝炎, 免疫机制, 信号通路

Abstract: Autoimmune hepatitis (AIH) is a chronic, inflammatory liver disease mediated by the immune system. Due to a breakdown in immune tolerance to liver autoantigens, multiple immune cells become activated and release abundant inflammatory factors. These autoantigens and inflammatory factors act upon cell surface receptors, activating multiple signaling pathways, including NF-κB, AMPK, PI3K/Akt, JAK/STAT, and MAPK, which induce or exacerbate immune-mediated liver injury. This occurs through the modulation of various processes in immune cells (such as dendritic cells, macrophages, and T cells), including energy metabolism, autophagy, apoptosis, and receptor expression.

Key words: autoimmune hepatitis, immune mechanism, signaling pathway

中图分类号:

R575

王倩辰, 万鹏, 任鑫瑶, 王阳阳. 自身免疫性肝炎发病机制的研究进展[J]. 基础医学与临床, 2026, 46(8): 1135-1138.

WANG Qianchen, WAN Peng, REN Xinyao, WANG Yangyang. The progress on the pathogenesis of autoimmune hepatitis[J]. Basic & Clinical Medicine, 2026, 46(8): 1135-1138.

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自身免疫性肝炎发病机制的研究进展

The progress on the pathogenesis of autoimmune hepatitis

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