Abstract
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.
Highlights
Glaucoma is one of the leading causes of blindness worldwide
Increased intraocular pressure is considered a major risk factor [3,4,5,6,7], numerous studies have suggested that glaucomatous neuropathy involves multiple factors, including impaired intraocular blood circulation [8,9,10,11], excitotoxic reactions caused by excess accumulation of glutamate [11,12,13], free
Subjects who satisfied the following criteria were enrolled: (1) a decrease in neuroretinal rim width to less than or equal to 0.1 of the cup-to-disc ratio or glaucomatous optic neuropathy diagnosed by an experienced glaucoma specialist; (2) a reliable and reproducible Humphrey visual field defect of greater than 5 dB in at least two points or greater than10 dB in a single point below age-specific normal threshold; (3) a mandatory diagnosis of exclusive NTG, primary open-angle closure (POAG), or chronic angle-closure glaucoma (CACG)
Summary
Glaucoma is one of the leading causes of blindness worldwide. It includes chronic neurodegenerative diseases of the optic nerve such as apoptosis of retinal ganglion cells (RGCs), progressive loss of optic nerve axons, and visual fields defects [1,2]. Th1/Th2 Cytokine Imbalance in the Iris of Patients with Glaucoma radical production and oxidative stress [14,15,16,17], increased NO levels [18,19,20], and immunological factors. What’s more, the advances and understanding made in both animal models of glaucoma as well as in human glaucoma autopsy findings in the 90’s and 00’s suggests there is a fundamental role of the immune system in mediating neuronal cell death in glaucoma regardless of intraocular pressure [102,103,104]
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