Increased Th1/Th17 Responses Contribute to Low-Grade Inflammation in Age-Related Macular Degeneration

被引:37
作者
Chen, Jiajia [1 ]
Wang, Wenzhan [1 ]
Li, Qiuming [2 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Ophthalmol 1, Zhengzhou, Henan, Peoples R China
[2] Zhengzhou Univ, Affiliated Hosp 1, Dept Ophthalmol 2, 1 Jianshe East Rd, Zhengzhou, Henan, Peoples R China
关键词
Age-related macular degeneration; Th1; Th17; ADAPTIVE IMMUNITY; EPITHELIAL-CELLS; EXPRESSION; MONOCYTES; MACROPHAGES; INDUCTION; UVEITIS;
D O I
10.1159/000484907
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background/Aims: Age-related macular degeneration (AMD) is the primary cause of senior blindness in developed countries. Mechanisms underlying initiation and development of AMD remained known. Methods: We examined the CD4(+) T cell compartments and their functions in AMD patients. Results: AMD patients presented significantly higher frequencies of interferon (IFN)-gamma-expressing and interleukin (IL)-17-expressing CD4(+) T cells than healthy controls. The levels of IFN-gamma and IL-17 expression by CD4(+) T cells were significantly higher in AMD patients. These IFN-gamma-expressing Th1 cells and IL-17-expressing Th17 cells could be selectively enriched by surface CCR3(+) and CCR4(+) CCR6(+) expression, respectively. Th1 and Th17 cells from AMD patients promoted the differentiation of monocytes toward M1 macrophages, which were previously associated with retinal damage. Th1 and Th17 cells also increased the level of MHC class I expression in human retinal pigment epithelial (RPE)-1 cells, while Th1 cells increased the frequency of MHC class II-expressing RPE-1 cells. These proinflammatory effects were partly, but not entirely, induced by the secretion of IFN-gamma and IL-17. Conclusions: This study demonstrated an enrichment of Th1 cells and Th17 cells in AMD patients. These Th1 and Th17 cells possessed proinflammatory roles in an IFN-gamma- and IL-17-dependent fashion, and could potentially serve as therapeutic targets. (c) 2017 The Author(s) Published by S. Karger AG, Basel
引用
收藏
页码:357 / 367
页数:11
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