Most patients with chronic dry eye disease (DED) have episodic flares, which can be triggered by a variety of activities and environmental stresses. These flares are typically associated with rapid exacerbation of discomfort symptoms, followed by prolonged elevation of inflammation. In an acute flare, ocular surface inflammation begins with a nonspecific innate immune response, in some cases followed by a slower but more specific adaptive immune response. At the ocular surface, epithelial cells are central to the innate immune response, and we discuss their role in DED flares alongside the other core components. Epithelial cells and other cells of the innate response (neutrophils, monocytes, macrophages and dendritic cells) trigger flares in response to increased osmolarity, detected via pattern receptors on their cell surface. Ultimately, downstream signaling pathways activate innate and adaptive immune responses, with consequent inflammation and symptoms. In chronic DED, pathogenic T cells have infiltrated the ocular surface tissues. The established adaptive immune response is likely to lead to flare-ups at lower thresholds of stress, with inflammation maintained over a longer period. Increased understanding of the inflammatory cascades activated during a flare may guide management and improve outcomes.

大多数慢性干眼病 (DED) 患者都会出现间歇性症状，可能是由各种活动和环境压力引发的。这些耀斑通常与不适症状的快速恶化有关，随后是炎症的长期加剧。在急性发作中，眼表炎症始于非特异性先天免疫反应，在某些情况下随后出现较慢但更特异性的适应性免疫反应。在眼表，上皮细胞是先天免疫反应的核心，我们与其他核心成分一起讨论它们在 DED 发作中的作用。上皮细胞和其他先天反应细胞（中性粒细胞、单核细胞、巨噬细胞和树突细胞）会因渗透压增加而引发耀斑，这是通过细胞表面的模式受体检测到的。最终，下游信号通路激活先天性和适应性免疫反应，从而产生炎症和症状。在慢性 DED 中，致病性 T 细胞已浸润眼表组织。已建立的适应性免疫反应可能会导致在较低压力阈值下突然爆发，并且炎症会维持较长时间。增加对发作期间激活的炎症级联的了解可以指导管理并改善结果。