The mechanistic study of glaucoma pathogenesis has shifted to seeking to understand the effects of immune responses on retinal ganglion cell damage and protection. Cytokines mediate the biological effects of the immune system, and our previous study revealed an imbalance of T-helper (Th) 1-derived and Th2-derived cytokines in the serum of patients with glaucoma. In this study, we collected irises from normal individuals and patients with primary open-angle closure (POAG) or chronic angle-closure glaucoma (CACG). We used real-time polymerase chain reaction (PCR) to measure the expression of Th1 (interleukin (IL)-2, interferon-gamma (IFN-γ)), Th2 (IL-4, IL-6, IL-10), and Th3 (transforming growth factor-beta (TGF-β)) cytokines. We then performed immunohistochemical staining to characterize the localization of the upregulated cytokines in iris cryosections. We observed an upward trend in the expression of IL-2 and IFN-γ and a downward trend in IL-6 expression in the iris of POAG and CACG patients. Expression of TGF-β also increased. Immunohistochemistry revealed that IL-2 expression in POAG and CACG patients was localized in the anterior surface of the blood vessel wall in the stroma of the iris, in the cytoplasm of some cells, in the anterior epithelium, and in the posterior pigment epithelium. These findings indicate that immune status differed between the iris tissues of POAG and CACG patients and those of normal individuals. A T-helper cytokine imbalance may modulate the immune microenvironment in glaucomatous eyes and thus influence optic neuropathy.
青光眼发病机制的机制研究已转向寻求了解免疫反应对视网膜神经节细胞损伤和保护的影响。细胞因子介导免疫系统的生物学效应,我们之前的研究揭示了青光眼患者血清中辅助性T细胞(Th)1型和Th2型细胞因子的失衡。在这项研究中,我们收集了正常个体以及原发性开角型青光眼(POAG)或慢性闭角型青光眼(CACG)患者的虹膜。我们使用实时聚合酶链反应(PCR)来测量Th1(白细胞介素(IL)-2、干扰素 -γ(IFN -γ))、Th2(IL - 4、IL - 6、IL - 10)和Th3(转化生长因子 -β(TGF -β))细胞因子的表达。然后我们进行免疫组织化学染色以确定上调的细胞因子在虹膜冰冻切片中的定位。我们观察到POAG和CACG患者虹膜中IL - 2和IFN -γ的表达呈上升趋势,IL - 6的表达呈下降趋势。TGF -β的表达也增加了。免疫组织化学显示,POAG和CACG患者中IL - 2的表达定位于虹膜基质中血管壁的前表面、一些细胞的细胞质、前上皮以及后色素上皮。这些发现表明,POAG和CACG患者的虹膜组织与正常个体之间的免疫状态不同。辅助性T细胞因子失衡可能调节青光眼眼中的免疫微环境,从而影响视神经病变。