免疫失调在过敏性结膜炎的发生和进展中扮演关键角色。本文对针刺治疗过敏性结膜炎的相关机制进行系统综述。首先，本文探讨了过敏性结膜炎的发病机制，重点分析免疫细胞（肥大细胞、巨噬细胞、T细胞、嗜酸性粒细胞）在眼部超敏反应中的作用，发现Th2型免疫应答及其分泌的IL-4、IL-13等细胞因子能直接驱动IgE生成和炎症级联反应。然而，尽管已有较多研究基础，过敏性结膜炎中神经免疫交互机制及眼表微环境失衡的具体调控路径仍面临较大的挑战。其次，通过研究针刺对过敏性结膜炎的作用，发现针刺能够调控多种免疫细胞功能，包括稳定肥大细胞膜、诱导M2型巨噬细胞极化、调节T细胞亚群平衡，从而抑制眼部炎症表达。相关动物实验证实针刺对过敏性结膜炎的治疗效果。此外，针刺通过激活胆碱能抗炎通路（α7nAChR/NF-κB）及调控JAK1/STAT6信号通路，在调节神经免疫交互和减轻神经源性炎症方面表现出良好的干预效应，同时针刺还能促进泪液分泌、增加黏蛋白MUC5AC表达，改善眼表微环境。然而，针刺在这一过程中的具体分子机制及相关信号通路的网络整合尚未完全阐明。随着神经免疫学及代谢组学技术的不断发展，未来有望在过敏性结膜炎发病机制及针刺治疗机制研究方面取得新的突破。

针刺；过敏性结膜炎；免疫调节；神经免疫；眼表微环境

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