Abstract
Macrophages are involved in low-grade inflammation in diabetes, and play pathogenic roles in proliferative diabetic retinopathy (PDR) by producing proinflammatory cytokines. T cells as well as other cells are also activated by proinflammatory cytokines, and infiltration into the vitreous of patients with PDR has been shown. In this study, we measured helper T (Th) cell-related cytokines in the vitreous of PDR patients to define the characteristics of Th-mediated immune responses associated with PDR. The study group consisted of 25 type 2 diabetic patients (25 eyes) with PDR. The control group consisted of 27 patients with epiretinal membrane (ERM), 26 patients with idiopathic macular hole (MH), and 26 patients with uveitis associated with sarcoidosis. Vitreous fluid was obtained at the beginning of vitrectomy, and centrifuging for cellular removals was not performed. Serum was also collected from PDR patients. IL-1β, IL-4, IL-6, IL-10, IL-17A, IL-17F, IL-21, IL-22, IL-23, IL-25, IL-31, IL-33, IFN-γ, soluble sCD40L, and TNFα in the vitreous and serum samples were measured. Both percent detectable and levels of IL-4, IL-6, IL-17A, IL-21, IL-22, and TNFα in the vitreous were significantly higher than those in the serum in PDR patients. Vitreous levels of these cytokines and IL-31 were significantly higher in PDR than in ERM or MH patients. Vitreous levels of IL-4, IL-17A, IL-22, IL-31, and TNFα in PDR patients were also significantly higher than those of sarcoidosis patients. In PDR patients, vitreous IL-17A level correlated significantly with vitreous levels of IL-22 and IL-31, and especially with IL-4 and TNFα. Although it is unclear whether these cytokines play facilitative roles or inhibitory roles for the progression of PDR, the present study indicated that Th2- and Th17-related immune responses are involved in the pathogenesis of PDR.
Highlights
Diabetic retinopathy (DR) is one of the most serious complications of diabetes, and is potentially sight-threatening in patients aged 20–75 years [1]
Interleukin (IL)-1β [4], IL-6 [5], IL-8 [5], and tumor necrosis factor α (TNFα) [4] are known to be increased in the vitreous fluid of proliferative diabetic retinopathy (PDR) patients, and elevated vitreous levels of C-C motif ligand 2 (CCL2)/monocyte chemoattractant protein1 (MCP-1), C-X-C motif ligand (CXCL)4/platelet factor (PF)-4, CXCL9/monokine induced by gamma interferon (Mig), and CXCL10/interferon gamma-induced protein (IP)-10 in PDR patients have been reported [6]
Cytokines with percent detectable higher than 20% either in the serum or in the vitreous were IL-4, IL-6, IL-10, IL-17A, IL21, IL-22, IL-31, soluble CD40 ligand (sCD40L), and TNFα
Summary
Diabetic retinopathy (DR) is one of the most serious complications of diabetes, and is potentially sight-threatening in patients aged 20–75 years [1]. Th Cell-Related Cytokines and Proliferative Diabetic Retinopathy patients is higher than 40%, and approximately 5%- 10% of DR cases progress to severe visual impairment [1]. Several studies have indicated that inflammatory process is involved in the pathogenesis of DR provoking retinal tissue damage, and that progression of PDR is mediated by various systemic and local factors [2, 3]. Previous studies have demonstrated that macrophages are involved in low-grade inflammation in diabetes, and play pathogenic roles in PDR by producing or expressing the above factors [7, 8]. CD4+ and CD8+ T cells infiltrate the vitreous of PDR patient and the CD4/CD8 ratio is higher in the vitreous than in the blood [9, 10], the involvement of T cells in progression of PDR has not yet been elucidated
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