固有淋巴样细胞作为组织稳态的核心调节者：对过敏性疾病的意义

文献信息

中文摘要

屏障组织在维持免疫耐受和组织完整性的同时，持续遭遇环境挑战。皮肤、呼吸道和胃肠道黏膜内稳态的维持需要上皮细胞、基质细胞、神经元、血管和免疫细胞之间的协调通讯。固有淋巴样细胞（ILCs）因其在屏障组织内的战略性定位以及快速整合组织来源信号的能力，已成为这些过程的关键调节者。尽管最初被归类为辅助性T细胞亚群的固有对应物，但越来越多的证据表明，成熟ILC的身份持续受到发育编程、组织特异性环境线索和功能可塑性的塑造。除了其在宿主防御中的既定作用外，ILCs还通过与结构细胞和免疫细胞的广泛相互作用，调节上皮维持、组织修复、细胞外基质重塑、神经免疫通讯和炎症消退。在生理条件下，这些活动维持屏障完整性并在损伤后恢复组织稳态。然而，持续的上皮损伤和慢性环境刺激暴露会破坏这些调节网络，导致ILC持续活化、消退受损、病理性重塑和进行性器官功能障碍。本综述特别强调ILC2s在过敏性疾病中的作用，总结了ILC发育、组织适应和多细胞通讯方面的最新进展，并探讨了这些稳态程序的破坏如何促成哮喘、慢性鼻窦炎伴鼻息肉、嗜酸性粒细胞性胃肠道疾病和特应性皮炎。最后，我们重点介绍了可能促进以恢复组织稳态作为慢性过敏性疾病治疗策略的新兴技术和未来方向。

英文摘要

Barrier tissues continuously encounter environmental challenges while maintaining immune tolerance and tissue integrity. Preservation of homeostasis within the skin, respiratory tract, and gastrointestinal mucosa requires coordinated communication among epithelial, stromal, neuronal, vascular, and immune cells. Innate lymphoid cells (ILCs) have emerged as key regulators of these processes owing to their strategic localization within barrier tissues and their capacity to rapidly integrate tissue-derived signals. Although initially classified as innate counterparts of helper T-cell subsets, accumulating evidence demonstrates that mature ILC identity is continuously shaped by developmental programming, tissue-specific environmental cues, and functional plasticity. Beyond their established roles in host defense, ILCs regulate epithelial maintenance, tissue repair, extracellular matrix remodeling, neuroimmune communication, and resolution of inflammation through extensive interactions with structural and immune cells. Under physiological conditions, these activities preserve barrier integrity and restore tissue homeostasis following injury. However, persistent epithelial damage and chronic exposure to environmental stimuli disrupt these regulatory networks, resulting in sustained ILC activation, impaired resolution, pathological remodeling, and progressive organ dysfunction. With particular emphasis on ILC2s in allergic disease, this review summarizes recent advances in ILC development, tissue adaptation, and multicellular communication, and examines how disruption of these homeostatic programs contributes to asthma, chronic rhinosinusitis with nasal polyps, eosinophilic gastrointestinal diseases, and atopic dermatitis. Finally, we highlight emerging technologies and future directions that may facilitate restoration of tissue homeostasis as a therapeutic strategy for chronic allergic diseases.