固有淋巴样细胞在自身免疫性、过敏性和感染性疾病中的作用：一项系统综述

文献信息

中文摘要

固有淋巴样细胞（ILCs）是组织驻留免疫细胞，其功能与CD4+辅助性T（Th）1、Th2和Th17细胞相似，并据此分为ILC1、ILC2和ILC3。ILC家族的其他成员包括淋巴组织诱导（LTi）细胞和自然杀伤（NK）细胞。ILCs在屏障表面丰富存在，是病原体的首批应答者之一，参与组织稳态和适应性免疫。本系统综述遵循PRISMA指南进行，综合了关于ILCs在自身免疫性、过敏性和感染性疾病中的人类临床证据。通过主要数据库检索了截至2025年12月发表的相关同行评议文章。从2545条初始记录中，选择170篇进行全文评估，最终纳入135篇。研究结果异质性较大，最一致的证据表明：（i）在炎症性肠病（IBD）中，可塑性驱动的从保护性IL-22+ ILC3向致病性IFN-γ+ ILC1的转变损害了黏膜屏障完整性；（ii）在多发性硬化中，调节性CD56bright NK细胞的富集标志着临床成功，而第3组ILCs与脑膜异位淋巴新生有关；（iii）在系统性红斑狼疮中，扩增的IFN-γ+ ILC1s与疾病严重程度相关，并放大致病性I型干扰素反应；（iv）在过敏性疾病（哮喘、过敏性鼻炎和慢性鼻窦炎）中，活化的ILC2s驱动自我延续的炎症回路和组织重塑。未来的研究应解决异质性的潜在来源，并就ILCs在疾病发病机制中的作用达成共识，以增强其作为新型诊断和治疗策略靶点的潜力。

英文摘要

Innate lymphoid cells (ILCs) are tissue-resident immune cells that functionally mirror CD4+ T helper (Th)1, Th2 and Th17 cells, and are accordingly classified as ILC1, ILC2 and ILC3. Additional members of the ILC family include lymphoid tissue inducer (LTi) cells and natural killer (NK) cells. Abundant at barrier surfaces, ILCs are among the first responders to pathogens, contributing to tissue homeostasis and adaptive immunity. This systematic review, conducted following PRISMA guidelines, synthesises human clinical evidence on ILCs in autoimmune, allergic and infectious diseases. Relevant peer-reviewed articles published up to December 2025 were identified across major databases. From 2545 initial records, 170 were selected for full-text evaluation and 135 were ultimately included. Findings were heterogeneous, with the most consistent evidence demonstrating: (i) in inflammatory bowel disease (IBD), a plasticity-driven shift from protective IL-22+ ILC3s to pathogenic IFN-γ+ ILC1s compromises mucosal barrier integrity; (ii) in multiple sclerosis, enrichment of regulatory CD56bright NK cells marks clinical success, while Group 3 ILCs are implicated in meningeal ectopic lymphoid neogenesis; (iii) in systemic lupus erythematosus, expanded IFN-γ+ ILC1s correlate with disease severity and amplify pathogenic Type I interferon responses; and (iv) in allergic diseases (asthma, allergic rhinitis and chronic rhinosinusitis), activated ILC2s drive self-perpetuating inflammatory circuits and tissue remodelling. Future studies should address potential sources of heterogeneity and establish a consensus regarding the role of ILCs in disease pathogenesis to enhance their potential as targets for novel diagnostic and therapeutic strategies.