干性年龄相关性黄斑变性中的炎症

Inflammation in dry age-related macular degeneration.

作者信息

Rodrigues Eduardo B

机构信息

Retina Department, Ophthalmology Service, Hospital Regional São José, Instituto de Olhos Florianópolis/Centro Oftalmológico, Florianópolis, Brazil.

出版信息

Ophthalmologica. 2007;221(3):143-52. doi: 10.1159/000099293.

DOI:10.1159/000099293

PMID:17440275

Abstract

PURPOSE

To summarize the current information regarding the role of immune and inflammatory response in the pathogenesis of dry age-related macular degeneration (ARMD).

METHODS

A Pubmed search was conducted of the period January 1999 to 2005. Relevant information in the literature on the role of inflammation in early dry ARMD was reviewed.

RESULTS

Some important evidence for inflammation in early ARMD consists in the isolation of immunoglobulins, complement proteins, cytokines and activated microglia, in retinal pigment epithelium (RPE) cells and drusen. Pivotal mechanisms in early ARMD include the accumulation of debris and proteins along the RPE surface, followed by immune-complex deposition and complement activation. In contrast, the role of other plasma enzymes such as kallikrein-kinin-bradykinin, the Hageman factor, peptides and coagulation proteins in drusen formation and ARMD has yet to be determined.

CONCLUSION

A clear role for inflammatory mediators and cells has been established in recent years. Future studies should elucidate further mechanisms in ARMD development.

摘要

目的

总结目前关于免疫和炎症反应在干性年龄相关性黄斑变性（ARMD）发病机制中作用的信息。

方法

对1999年1月至2005年期间进行了PubMed检索。回顾了文献中关于炎症在早期干性ARMD中作用的相关信息。

结果

早期ARMD中炎症的一些重要证据包括在视网膜色素上皮（RPE）细胞和玻璃膜疣中分离出免疫球蛋白、补体蛋白、细胞因子和活化的小胶质细胞。早期ARMD的关键机制包括RPE表面碎片和蛋白质的积累，随后是免疫复合物沉积和补体激活。相比之下，其他血浆酶如激肽释放酶-激肽-缓激肽、Hageman因子、肽和凝血蛋白在玻璃膜疣形成和ARMD中的作用尚未确定。