The IL-23/IL-17 axis promotes the formation of retinal neovascularization by activating the NLRP3 inflammasome in macrophages in an experimental retinopathy mouse model,Immunology

当前位置： X-MOL 学术 › Immunology › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

The IL-23/IL-17 axis promotes the formation of retinal neovascularization by activating the NLRP3 inflammasome in macrophages in an experimental retinopathy mouse model
Immunology ( IF 4.9 ) Pub Date : 2021-08-15 , DOI: 10.1111/imm.13402
Ailing Sui ₁ , Xiuping Chen ₂ , Yiyun Yao ₁ , Yixuan Yao ₁ , Xi Shen ₁ , Yanji Zhu ₁ , Bing Xie ₁

Affiliation

Retinal neovascularization (RNV), a pathological process shared among diabetic retinopathy, retinopathy of prematurity and other retinopathies, has been widely studied, but the mechanism remains unclear. In this study, the mechanism by which the interleukin (IL)-23/IL-17 axis regulates RNV in oxygen-induced retinopathy (OIR) model mice and in cell experiments in vitro was characterized. In the retinas of OIR mice, IL-23/IL-17 axis activation was increased and regulated RNV formation, and this effect was accompanied by increased macrophage recruitment and nucleotide-binding domain leucine-rich repeat and pyrin domain containing receptor 3 (NLRP3) inflammasome activation. Moreover, inhibiting the IL-23/IL-17 axis reduced the number of macrophage and the expression and activation of NLRP3 inflammasome. On the other hand, recombinant (r) IL-23p19 and rIL-17A promoted the expression and activation of NLRP3 inflammasome, and the proliferation and migration of macrophages. Furthermore, macrophage elimination decreased the activation of IL-23/IL-17 axis and the expression and activation of NLRP3 inflammasome. In summary, our experiments showed that the IL-23/IL-17 axis promoted the formation of RNV by activating the NLRP3 inflammasome in retinal macrophages of an OIR mouse model.

中文翻译：

在实验性视网膜病变小鼠模型中，IL-23/IL-17 轴通过激活巨噬细胞中的 NLRP3 炎性体促进视网膜新生血管的形成

视网膜新生血管形成（RNV）是糖尿病视网膜病变、早产儿视网膜病变和其他视网膜病变共有的病理过程，已被广泛研究，但其机制仍不清楚。在这项研究中，白细胞介素 (IL)-23/IL-17 轴在氧诱导视网膜病变 (OIR) 模型小鼠和体外细胞实验中调节 RNV 的机制得到了表征。在 OIR 小鼠的视网膜中，IL-23/IL-17 轴激活增加并调节 RNV 形成，这种效应伴随着巨噬细胞募集和核苷酸结合域富含亮氨酸重复序列和含有受体 3 (NLRP3) 的热蛋白结构域的增加炎性小体激活。此外，抑制 IL-23/IL-17 轴可减少巨噬细胞的数量以及 NLRP3 炎性体的表达和激活。另一方面，重组 (r) IL-23p19 和 rIL-17A 促进 NLRP3 炎性体的表达和激活，以及巨噬细胞的增殖和迁移。此外，巨噬细胞消除减少了 IL-23/IL-17 轴的激活以及 NLRP3 炎性体的表达和激活。总之，我们的实验表明，IL-23/IL-17 轴通过激活 OIR 小鼠模型视网膜巨噬细胞中的 NLRP3 炎性体来促进 RNV 的形成。

更新日期：2021-08-15

点击分享查看原文

点击收藏

阅读更多本刊最新论文本刊介绍/投稿指南11