Elnaz Taghvaei-Bijandi; Fatemeh Abedian; Ahmad Ahmadzadeh Amiri; Narjes Jafari; Saeid Abediankenari
Abstract
Background: Retinopathy of diabetes is a chronic diabetes mellitus complication affecting retinal vessels, and some ocular complications’ molecular mechanisms remain obscure.Objective: To evaluate the expression of HLA-G1, HLA-G5, miRNA-181a, and miRNA-34a in the lens epithelial cells of patients ...
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Background: Retinopathy of diabetes is a chronic diabetes mellitus complication affecting retinal vessels, and some ocular complications’ molecular mechanisms remain obscure.Objective: To evaluate the expression of HLA-G1, HLA-G5, miRNA-181a, and miRNA-34a in the lens epithelial cells of patients with retinopathy of diabetes.Methods: In a case-control study, 30 diabetic patients with retinopathy, 30 diabetic patients without retinopathy, and 30 cataract patients without diabetes mellitus as the control group were enrolled after a full description with details about the study methods and objectives. The expression of HLA G1, HLA G5, miRNA-181a, and miRNA-34a in lens epithelial cells was assessed by quantitative RT PCR. Moreover, the levels of HLA-G protein in aqueous humor were evaluated by the ELISA method.Results: HLA-G1 expression was significantly upregulated in the retinopathy group (P=0.003). The aqueous humor of diabetic retinopathy patients contained significantly higher levels of HLA-G protein compared with the non-diabetic patients (P=0.001). miRNA-181a was significantly downregulated in the diabetic retinopathy group compared with the patients without diabetes (P=0.001). In addition, miRNA-34a was upregulated in the retinopathy group (P=0.009).Conclusion: Taken together, the present results showed that HLA-G1 and miRNA-34a can be valuable markers for diabetic retinopathy. Our data offers new perspectives for improving the control of inflammation in the lens epithelial cells by considering HLA-G and miRNA.
Mehran Ahmadi; Abdolkarim Mahrooz; Saeid Abediankenari; Nasim Hayati Roodbari
Abstract
Background: Functional single nucleotide polymorphisms in zinc transporter 8 (ZnT8) gene may be key determinants of humoral autoreactivity to ZnT8. Objective: The present study is expected to provide new information on the association of rs11558471 in ZnT8 gene with IL-17 levels and insulin resistance ...
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Background: Functional single nucleotide polymorphisms in zinc transporter 8 (ZnT8) gene may be key determinants of humoral autoreactivity to ZnT8. Objective: The present study is expected to provide new information on the association of rs11558471 in ZnT8 gene with IL-17 levels and insulin resistance in an Iranian population [a high-risk population for type 2 diabetes (T2D)]. Methods: A total of 133 patients with T2D and 128 control subjects were included. Insulin and IL-17 concentrations were determined using ELISA. Insulin and fasting glucose levels were used to determine homeostasis model assessment for insulin resistance (HOMA-IR). The genetic analyses were performed by the restricted fragment length polymorphism (RFLP) after PCR amplification. Results: The risk allele frequency of rs11558471 in this Iranian population was among the highest in different populations. In T2D patients, compared with the GG genotypes, IL-17 concentrations were significantly higher in the GA+AA group (p= 0.042). According to the genotypes of this SNP, IL-17 concentrations, fasting glucose and HOMA-IR increased with the following order:GG
Saeid Abediankenari; Davoud Shaker; Farshideh Abedian; Arazmohammad Mirabi
Volume 6, Issue 2 , June 2009, , Pages 61-66
Abstract
Background: Dendritic cells (DC) are a key regulator of the immune response, and interferon- beta (IFN-β) is considered an immunomodulatory molecule for DC. Objective: The purpose of this study was to evaluate the ability of IFN-β treated DC to induce cytokine secretion by CD4+ T cells. Methods: ...
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Background: Dendritic cells (DC) are a key regulator of the immune response, and interferon- beta (IFN-β) is considered an immunomodulatory molecule for DC. Objective: The purpose of this study was to evaluate the ability of IFN-β treated DC to induce cytokine secretion by CD4+ T cells. Methods: Dendritic cells were generated from blood monocytes with granulocyte-monocyte colony-stimulating factor and interleukin-4 with or without IFN-β. We analyzed the production of CD4+ T helper cytokines (IL-17, IFN- γ and IL-10) in the supernatant of the dendritic cell-T cell co- cultures by ELISA. We also studied the effects of HLA-G and costimulatory molecules on immature and mature DC. Results: IFN-γ and IL-17 decreased significantly in the presence of HLA-Gbearing DC compared to control cultures (p<0.05). Conclusion: Using the mixed leukocyte reaction, we found that DC treated with IFN-β mediated the inhibition of T cell activation via cytokine production. We conclude that this is important for preventing overactivation of the immune system.