过敏性结膜炎经典的发病机制包括了IgE介导的I型超敏反应以及T淋巴细胞介导的IV型超敏反应，其中肥大细胞、肥大细胞脱颗粒释放的组胺、嗜酸性粒细胞等在过敏性结膜炎病理发展中发挥了重要作用。然而，临床发现针对上述机制的治疗药物临床疗效欠佳，有相当数量的过敏性结膜炎患者无法获得较好的生存质量，因此研究和阐明过敏性结膜炎的新机制，寻找新的治疗手段和药物靶点具有重要的临床意义。目前研究发现Th17细胞等多种炎性细胞和IL-17等细胞因子、过敏原介导神经调节机制、菌群失调机制、脂质介质作用方面可能与过敏性结膜炎发病相关，这对过敏性结膜炎新机制的研究有着重大的临床意义。本文将对过敏性结膜炎发病机制的新进展进行综述，以期为过敏性结膜炎的治疗提供新思路。

The classic pathogeneses of allergic conjunctivitis include type I hypersensitivity and type IV hypersensitivity, in which mast cells, eosinophils and some active substances such as histamine play important role. However, sincethe therapeutic drugs have not achieved satisfactory efficacy in clinical practices, a significant number of patients fail to achieve a good quality of life. The pathogenesis of allergic conjunctivitis remains to be further studied.Current studies have identified a variety of inflammatory cells such as Th17 cell and cytokines such as IL-17, the mechanisms of neuromodulation, flora dysregulation mechanisms, and lipid mediators that may be involved in the pathogenesis of allergic conjunctivitis, which has significant clinical implications for the study of mechanisms of allergic conjunctivitis. In this article, we will review the recent research progress of the pathogenesis of allergic conjunctivitis in order to provide new ideas for the treatment of allergic conjunctivitis.