Diabetes-mediated IL-17A enhances retinal inflammation, oxidative stress, and vascular permeability

被引：50

作者：

Sigurdardottir, Sigrun ^{[1
]}

Zapadka, Thomas E. ^{[1
]}

Lindstrom, Sarah, I ^{[1
]}

Liu, Haitao ^{[2
]}

Taylor, Brooklyn E. ^{[1
]}

Lee, Chieh A. ^{[2
]}

Kern, Timothy S. ^{[2
,3
]}

Taylor, Patricia R. ^{[1
,3
]}

机构：

[1] Case Western Reserve Univ, Sch Med, Dept Ophthalmol & Visual Sci, Cleveland, OH USA

[2] Case Western Reserve Univ, Sch Med, Dept Pharmacol, Cleveland, OH USA

[3] Louis Stokes VA Med Ctr, Cleveland, OH USA

来源：

CELLULAR IMMUNOLOGY | 2019年 / 341卷

关键词：

IL-17A; Diabetic retinopathy; Retinal pathology; PHOTORECEPTOR CELLS; FUNCTIONAL LESIONS; T-ANTIGEN; RETINOPATHY;

D O I：

10.1016/j.cellimm.2019.04.009

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Diabetic retinopathy is a prevailing diabetes complication, and one of the leading causes of blindness worldwide. IL-17A is a cytokine involved in the onset of diabetic complications. In the current study, we examined the role of IL-17A in the development of retinal inflammation and long-term vascular pathology in diabetic mice. We found IL-17A expressing T cells and neutrophils in the retinal vasculature. Further, the IL-17A receptor was expressed on Muller glia, retinal endothelial cells, and photoreceptors. Finally, diabetes-mediated retinal inflammation, oxidative stress, and vascular leakage were all significantly lower in IL-17A(-/-) mice. These are all clinically meaningful abnormalities that characterize the onset of diabetic retinopathy.

引用

页数：6