Microglia in the outer retina and their relevance to pathogenesis of age-related macular degeneration.
Microglia in the outer retina and their relevance to pathogenesis of age-related macular degeneration.
复制标题
DOI：
10.1007/978-1-4614-0631-0_6
复制
发表时间：
2012
影响因子：
--
通讯作者：
Wong WT
中科院分区：
文献类型：
--
作者：
Ma W;Zhao L;Wong WT
视网膜相关性黄斑变性（AMD）是西方世界老年人法律的失明的最大原因，是一种其发病机制尚未完全理解并且仍然存在治疗挑战的疾病。AMD的病因被认为涉及视网膜的慢性神经炎症，但相关细胞机制的细节仍不完全清楚。视网膜小胶质细胞是视网膜中的主要常驻免疫细胞，并且通常不存在于外部视网膜（AMD的位点）中。它们在高龄和疾病条件下迁移和浸润到外层视网膜中暗示它们参与AMD的神经炎性病因。我们提出视网膜下腔中小胶质细胞和RPE细胞之间的相互作用导致RPE细胞的结构和生理学的显著改变，从而将视网膜-脉络膜界面的环境转变为有利于AMD进展和进展的环境。特别地，小胶质细胞诱导RPE改变，其导致更具化学吸引力、促炎性和促血管生成的环境，其增加免疫细胞的募集和活化并促进新生血管生长到视网膜中。小胶质细胞对RPE的影响可能代表细胞与细胞的相互作用，这种相互作用可能是治疗和/或预防AMD的治疗策略的目标。
Age-related macular degeneration (AMD), the largest cause of legal blindness in the elderly in the Western world, is a disease whose pathogenesis is incompletely understood and for which therapeutic challenges remain. The etiology of AMD is thought to involve chronic neuroinflammation of the retina but the details of relevant cellular mechanisms are still not fully understood. Retinal microglia are the primary resident immune cell in the retina and are normally absent from the outer retina, the locus of AMD. Their migration and infiltration into the outer retina under conditions of advanced age and disease implicate their involvement in the neuroinflammatory etiology of AMD. We propose that interactions between microglia and RPE cells in the subretinal space result in significant alterations in the structure and physiology of RPE cells that in turn transforms the environment of the retino-choroidal interface into one conducive for the progression and advancement of AMD. In particular, microglia induce RPE alterations that result in a more chemoattractive, pro-inflammatory, and pro-angiogenic environment that increases the recruitment and activation of immune cells and fosters the growth of neovascular vessels into the retina. Microglia-to-RPE influences may represent a cell-cell interaction that may be targeted for therapeutic strategies to treat and/or prevent AMD.