Ocular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, 6565 Fannin NC205, Houston, TX 77030, USA.
Exp Eye Res. 2013 Dec;117:118-25. doi: 10.1016/j.exer.2013.08.013. Epub 2013 Sep 4.
Dry eye is an inflammatory disease that results from activation of innate inflammatory pathways in resident ocular surface cells, as well as cytokines produced by recruited T helper (Th) cells. Cytokines produced by the infiltrating Th cells alter the normal cytokine balance on the ocular surface and cause ocular surface epithelial pathology. Changes in levels of Th cytokines on the ocular surface have been measured in dry eye and the biological effects of these cytokines have been documented in experimental culture and mouse model systems. The Th2 cytokine IL-13 has a homeostatic role in promoting goblet cell differentiation. In contrast, The Th1 cytokine IFN-γ antagonizes IL-13 and promotes apoptosis and squamous metaplasia of the ocular surface epithelia. The Th17 cytokine, IL-17 promotes corneal epithelial barrier disruption. The ocular surface epithelium expresses receptors to all of these Th cytokines. Therapies that maintain normal IL-13 signaling, or suppress IFN-γ and IL-17 have potential for treating the ocular surface disease of dry eye.
干眼症是一种炎症性疾病，其发生是由于固有炎症途径在常驻眼表细胞中被激活，以及募集的辅助性 T 细胞 (Th) 产生的细胞因子所致。浸润的 Th 细胞产生的细胞因子改变了眼表的正常细胞因子平衡，并导致眼表上皮病理学改变。在干眼症中已经测量了眼表 Th 细胞因子水平的变化，并且已经在实验培养和小鼠模型系统中记录了这些细胞因子的生物学效应。Th2 细胞因子 IL-13 在促进杯状细胞分化方面具有稳态作用。相比之下，Th1 细胞因子 IFN-γ 拮抗 IL-13 并促进眼表上皮的凋亡和鳞状化生。Th17 细胞因子 IL-17 促进角膜上皮屏障破坏。眼表面上皮表达所有这些 Th 细胞因子的受体。维持正常 IL-13 信号传导或抑制 IFN-γ 和 IL-17 的疗法具有治疗干眼症眼表疾病的潜力。
