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
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
收藏
页数:6
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