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白细胞介素 35 调节增殖性糖尿病性视网膜病变患者白细胞介素 17 的表达和辅助性 T 细胞 17。

Interleukin 35 regulates interleukin 17 expression and T helper 17 in patients with proliferative diabetic retinopathy.

机构信息

Department of Ophthalmology, The First People's Hospital of Zunyi, The Third Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China.

出版信息

Bioengineered. 2022 May;13(5):13293-13299. doi: 10.1080/21655979.2022.2080367.

DOI:10.1080/21655979.2022.2080367
PMID:35635032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9275983/
Abstract

T helper 17 (Th17) cells regulate inflammatory processes and are implicated in pathogenesis of proliferative diabetic retinopathy (PDR) through modulation of interleukin-17 (IL-17). IL-35, anti-inflammatory factor, negatively mediates IL-17 expression and Th17 differentiation. In this study, the role of IL-35 in PDR was assessed. The results showed that IL-35 was down-regulated, while IL-17 was up-regulated, in peripheral blood mononuclear cells (PBMCs) of PDR patients. In addition, immunofluorescence analysis indicated that frequency of Th17 cells was enhanced in the PBMCs of PDR patients. However, incubation with IL-35 reduced the Th17 cell frequency and decreased the level of IL-17 in CD4 T lymphocytes. Moreover, the levels of transcription factors essential for Th17 differentiation, ROR α (retinoid-related orphan receptor alpha) and ROR γt, were reduced by IL-35 treatment. In conclusion, IL-35 reduced level of IL-17 and inhibited Th17 differentiation to protect against PDR.

摘要

辅助性 T 细胞 17(Th17)细胞调节炎症过程,并通过调节白细胞介素-17(IL-17)参与增殖性糖尿病视网膜病变(PDR)的发病机制。抗炎因子 IL-35 通过负向调节 IL-17 的表达和 Th17 分化来发挥作用。本研究评估了 IL-35 在 PDR 中的作用。结果表明,PDR 患者外周血单个核细胞(PBMCs)中 IL-35 下调,而 IL-17 上调。此外,免疫荧光分析表明,PDR 患者 PBMCs 中的 Th17 细胞频率增加。然而,IL-35 孵育可降低 Th17 细胞频率,并降低 CD4 T 淋巴细胞中 IL-17 的水平。此外,IL-35 处理可降低 Th17 分化所必需的转录因子 RORα(维甲酸相关孤儿受体α)和 RORγt 的水平。综上所述,IL-35 降低了 IL-17 的水平,并抑制了 Th17 分化,从而起到了预防 PDR 的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa1d/9275983/17de5b8798c3/KBIE_A_2080367_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa1d/9275983/72dc23eea5ee/KBIE_A_2080367_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa1d/9275983/15b9c4c68c68/KBIE_A_2080367_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa1d/9275983/17de5b8798c3/KBIE_A_2080367_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa1d/9275983/72dc23eea5ee/KBIE_A_2080367_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa1d/9275983/15b9c4c68c68/KBIE_A_2080367_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa1d/9275983/17de5b8798c3/KBIE_A_2080367_F0003_B.jpg

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