在炎症性肠病中肠表皮和免疫微环境之间的双向交叉:机制和治疗影响
Jinghan Shen1, Simin Du1, Yuyue Zhang1
1School and Hospital of Stomatology, Zunyi Medical University, Zunyi, Guizhou, People's Republic of China.
Journal of inflammation research
|March 16, 2026
概括
这篇评论详细介绍了肠道屏障功能障碍和免疫失调如何驱动炎症性肠病 (IBD). 了解这些相互作用是开发IBD患者精密疗法的关键.
科学领域:
- 胃肠道学和免疫学
- 细胞生物学和分子医学
背景情况:
- 炎症性肠病 (IBD) 涉及慢性肠炎症,由肠上皮细胞 (IEC) 和免疫细胞之间的异常相互作用引起.
- 表皮屏障完整性和免疫微环境因素是IBD病原体的核心.
研究的目的:
- 系统地审查表皮屏障功能与IBD中的免疫调节之间的相互作用.
- 探索表皮损伤,修复和干细胞更新在IBD的机制.
- 评估IBD的新兴治疗策略和技术.
主要方法:
- 系统性文献综述,重点关注IBD中的上皮-免疫轴.
- 对关键分子通路的分析 (例如,NETosis,ROS/NOX4,IL-22/STAT3,Wnt/β-catenin,胆酸-TGR5).
- 整合来自单细胞奥米学,临床前模型和有机体研究的数据.
主要成果:
- 原生和适应性免疫细胞协调IBD炎症和粘膜修复.
- 特定的机制,如NETs,巨细胞两极分化和IL-22信号,对IBD具有关键的影响.
- Wnt/β-catenin和胆酸-TGR5通路对于肠道干细胞的更新至关重要.
- 新兴的疗法,如抗IL-23/IL-17生物制剂和MSC外体,显示出治疗潜力.
结论:
- 恢复免疫上皮质平衡需要对IBD进行精准医学方法.
- 有机器人为研究IBD机制和验证疗法提供了一个有希望的平台.
- 未来的研究应该专注于空间时间映射和双重目标疗法的翻译验证.
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