首页|NF-κB参与克罗恩病发生发展的机制

NF-κB参与克罗恩病发生发展的机制

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克罗恩病的发病率近年来有增高的趋势.核因子-kappaB(nuclear factor-kappa B,NF-κB)参与免疫反应的调控、炎症反应的发生和肠道稳态的维持,其异常激活是诱发或加重克罗恩病的重要危险因素.异常激活的NF-κB改变免疫细胞和肠道上皮细胞的功能状态,进而诱发慢性持续性肠道炎症和导致肠黏膜屏障受损.了解NF-κB和克罗恩病之间的关系可以为克罗恩病的预防及治疗提供有价值的思路.本文就NF-κB及其激活途径,NF-κB通过调节肠上皮细胞的功能、T辅助细胞分化、巨噬细胞极化、中性粒细胞凋亡和树突状细胞的成熟诱导克罗恩病的机制以及NF-κB在溃疡性结肠炎中的作用展开综述.
Mechanism of NF-κB participating in the occurrence and development of Crohn's disease
The incidence rate of Crohn's disease is increasing in recent years.Nuclear factor-kappa B(NF-κB)is involved in regulating immunity,inflammatory response and intestinal homeostasis.Its abnormal activation is an important risk factor for inducing or aggravating Crohn's disease.Abnormal activated NF-κB changes the functional status of immune cells and intestinal epithelial cells,and then induces chronic persistent intestinal inflammation and damages the intestinal mucosal barrier.Understand the relationship between NF-κB and Crohn's disease can provide valuable ideas for the prevention and treatment of Crohn's disease.This paper reviews NF-κB,activation pathway of NF-κB,the mechanism that NF-κB induces Crohn's disease by regulating the function of intestinal epithelial cells,T helper cell differentiation,macrophage polarization,neutrophil apoptosis and dendritic cell maturation,and the role of NF-κB in ulcerative colitis.

Crohn's diseasenuclear factor-kappa Bintestinal epithelial cellT helper cellmacrophage

陈威威、陈菲菲、柏文霞

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南京医科大学附属江宁医院,南京 211100

上海市养志康复医院(上海市阳光康复中心),上海 201619

克罗恩病 核因子-kappa B 肠道上皮细胞 T辅助细胞 巨噬细胞

南京市卫生科技发展一般性课题项目

YKK20196

2023

生命的化学
中国生物化学与分子生物学会

生命的化学

CSTPCD
影响因子:0.404
ISSN:1000-1336
年,卷(期):2023.43(10)
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