期刊文献+

青光眼与Th1、Th2相关细胞因子研究进展 被引量:2

Research progress of the related cytokines of Thl and Th2 on glaucoma
下载PDF
导出
摘要 青光眼是导致不可逆盲的首要原因,包括视野缺损和视神经的慢性退行性病变,如视网膜神经节细胞(RGCs)的凋亡和视神经轴突的逐步缺失。目前普遍认为高眼压是青光眼的主要危险因素,降低眼压是减缓青光眼发生和发展的首选治疗方法。近年来发现免疫因素是青光眼视神经损害的非压力依赖性危险因素之一。大部分免疫,甚至非免疫性生物效应都通过细胞因子来调控,而CD4+辅助性T细胞是细胞因子产生和调节的主要来源,其中Th1和Th2相关细胞因子在青光眼的发病机制中起着不可或缺的作用,并关系着RGCs的存活和凋亡。本文就近年Th1和Th2主要的相关细胞因子及Th1/Th2平衡与青光眼潜在关系的研究进展进行综述。 Glaucoma is a leading cause of irreversible blindness, which includes visual field defects and chronic degenerative diseases of the optic nerve, such as apoptosis of the retinal ganglion cells (RGCs) and progressive loss of optic nerve axons. Elevated intraocular pressure is the primary risk factor for glaucoma, and lowering intraocular pressure is the first choice of treatment for slowing the development of glaucoma. It has recently been found that immunological factors are one of the non-stress-dependent risk factors for optic nerve damage in glaucoma, while most of the immune and non-immune biological effects are regulated by cytokines. CD4+ helper T cells are the major sources of cytokines. Thl and Th2-related cytokines play an essential role in the pathogenesis of glaucoma and related with the survival and apoptosis of RGCs. In this review,we discussed the potential relationship between Thl/Th2-related cytokines and glaucoma.
作者 尚欢 张纯
出处 《中华实验眼科杂志》 CAS CSCD 北大核心 2017年第11期1052-1056,共5页 Chinese Journal Of Experimental Ophthalmology
基金 国家自然科学基金项目(81670851) 首都市民健康项目培育项目(Z151100003915143)
关键词 青光眼 细胞因子 CD4+辅助性T细胞 视神经损伤 Glaucoma Cytokines CD4+ helper T cells Optic nerve injury
  • 相关文献

参考文献4

二级参考文献50

  • 1卢华,马志中,刘敬,曹立群.视网膜脱离神经节细胞存活与IL-1β关系的实验研究[J].眼科研究,2005,23(3):286-289. 被引量:1
  • 2Moalem G,Yoles E,Leibowitz AR,et al.Autoimmune T cells retard the loss of function in injured rat optic nerves.J Neuroimmunol,2000,106:189-197.
  • 3Hauben E,Nevo U,Yoles E,et al.Autoimmune T cells as potential neuroprotective therapy for spinal cord injury.Lancet,2000,355:286-287.
  • 4Lü HZ,Xu L,Zou J,et al.Effects of autoimmunity on recovery of function in adult rats following spinal cord injury.Brain Behav Immun,2008,22:1217-1230.
  • 5London A,Itskovich E,Benhar I,et al.Neuroprotection and progenitor cell renewal in the injured aduh murine retina requires healing monocyte-derived macrophages.J Exp Med,2011,17:208:23-39.
  • 6Schwartz M.T cell-based vaccination against neunodegeneration:a new therapic approach.Retina J Ret Vit Dis,2005,25:33-35.
  • 7Bakalash S,Shilomo GB,Aloni E,et al.T-cell-based vaccination for morphological and functional neuroprotection in a rat model of chronically elevated intraocular pressure.J Mol Med,2005,83:904-916.
  • 8Yang B,Li S,Song W,et al.Copolymer-1 immunization reduces damage in retinal ganglion cells under high intraocular pressure through altering the expression of retinal neurotrophins.J Ocular Pharmacol Therap,2010,1:11-19.
  • 9Neuhaus O,Farina C,Yassouridis A,et al.Multiple sclerosis:comparison of copolymer-1-reactive T-cell lines from treated and untreated subjects reveals cytokine shift from T helper 1 to T helper 2 cells.Proc Natl Acad Sci USA,2000,97:7452-7457.
  • 10Aharoni R,Teietlbaum D,Sela M,et al.Copolymer 1 induces T cells of the T helper type 2 that crossreact with myelin basic protein and suppress experimental autoimmune encephalomyelitis.Proc Natl Acad Sci USA,1997,94:10821-10826.

共引文献10

同被引文献14

引证文献2

二级引证文献5

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部