不受欢迎却赖着不走：黄斑变性中存在缺陷的CX3CR1小胶质细胞受到关注。
Overstaying their welcome: defective CX3CR1 microglia eyed in macular degeneration.
作者信息
Chen Jing, Connor Kip M, Smith Lois E H
机构信息
Department of Ophthalmology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, USA.
出版信息
J Clin Invest. 2007 Oct;117(10):2758-62. doi: 10.1172/JCI33513.
Abstract
Age-related macular degeneration (AMD), the most common cause of blindness in the elderly, is characterized by degeneration of the macula and can lead to loss of fine color vision. Alterations in inflammatory and immune system pathways, which arise from genetic differences, predispose individuals to AMD. Yet the mechanism of disease progression with respect to inflammation is not fully understood. In this issue of the JCI, the study by Combadière and colleagues shows that CX3C chemokine receptor 1-deficient (CX3CR1-deficient) mice have abnormal microglia that accumulate beneath the retina and contribute to the progression of AMD.
摘要
年龄相关性黄斑变性（AMD）是老年人失明的最常见原因，其特征是黄斑变性，并可导致精细色觉丧失。由基因差异引起的炎症和免疫系统途径的改变使个体易患AMD。然而，关于炎症的疾病进展机制尚未完全了解。在本期《临床研究杂志》中，孔巴迪埃及其同事的研究表明，CX3C趋化因子受体1缺陷（CX3CR1缺陷）小鼠的小胶质细胞异常，这些细胞在视网膜下积聚并促进AMD的进展。
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