Yao Xin, Ma Kaiming, Zhu Yangzhuangzhuang, Cao Siyan
Division of Gastroenterology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Cells. 2025 Jun 2;14(11):825. doi: 10.3390/cells14110825.
Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is a chronic inflammatory disorder of the gastrointestinal tract with rising incidence and an unclear etiology. Innate lymphoid cells (ILCs) have recently emerged as key regulators of mucosal immunity and tissue homeostasis and are increasingly implicated in IBD. Unlike adaptive lymphocytes, ILCs do not require antigen recognition and clonal expansion to respond rapidly to environmental cues and shape immune responses. In a healthy gut, ILCs maintain intestinal homeostasis by guarding the epithelial barrier, protecting against pathogens, and mounting proper responses to external insults. However, their altered differentiation, proliferation, recruitment, activation, and interaction with other host cells, microbiota, and environmental stimuli may contribute to IBD. In this review, we discuss recent advances in understanding murine and human ILCs in the context of intestinal inflammation and IBD. A deeper understanding of ILC-mediated immune mechanisms may offer novel therapeutic strategies for restoring intestinal homeostasis and improving personalized management of IBD.
炎症性肠病(IBD),包括克罗恩病和溃疡性结肠炎,是一种胃肠道慢性炎症性疾病,发病率呈上升趋势且病因不明。固有淋巴细胞(ILC)最近已成为黏膜免疫和组织稳态的关键调节因子,并越来越多地与IBD相关联。与适应性淋巴细胞不同,ILC不需要抗原识别和克隆扩增就能快速响应环境信号并塑造免疫反应。在健康的肠道中,ILC通过保护上皮屏障、抵御病原体以及对外部损伤做出适当反应来维持肠道稳态。然而,它们分化、增殖、募集、激活的改变以及与其他宿主细胞、微生物群和环境刺激的相互作用可能导致IBD。在这篇综述中,我们讨论了在肠道炎症和IBD背景下对小鼠和人类ILC理解的最新进展。对ILC介导的免疫机制的更深入理解可能会为恢复肠道稳态和改善IBD的个性化管理提供新的治疗策略。
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