Kaarniranta K, Salminen A
Department of Ophthalmology, Institute of Clinical Medicine, University of Kuopio, P.O. Box 1627, 70211, Kuopio, Finland.
J Mol Med (Berl). 2009 Feb;87(2):117-23. doi: 10.1007/s00109-008-0418-z. Epub 2008 Nov 14.
Age-related macular degeneration (AMD) is the most common cause of irreversible loss of central vision. Histopathological studies have demonstrated that inflammation is the key player in the pathogenesis of AMD. Genetic studies have revealed that complement factor H is a strong risk factor for the development of AMD. However, innate immunity defence involves several other pattern recognition receptors (PRRs) which can trigger inflammatory responses. Retinal pigment epithelial (RPE) cells have the main role in the immune defence in macula. In this study, we examine in detail the endogenous danger signals which can activate different PRRs in RPE cells, such as Toll-like, NOD-like and scavenger receptors along with complement system. We also characterise the signalling pathways triggered by PRRs in evoking inflammatory responses. In addition, we will discuss whether AMD pathology could represent the outcome of chronic activation of the innate immunity defence in human macula.
年龄相关性黄斑变性（AMD）是导致中心视力不可逆丧失的最常见原因。组织病理学研究表明，炎症是AMD发病机制中的关键因素。遗传学研究显示，补体因子H是AMD发生发展的一个重要危险因素。然而，固有免疫防御涉及其他几种可引发炎症反应的模式识别受体（PRR）。视网膜色素上皮（RPE）细胞在黄斑区的免疫防御中起主要作用。在本研究中，我们详细研究了可激活RPE细胞中不同PRR的内源性危险信号，如Toll样、NOD样和清道夫受体以及补体系统。我们还对PRR引发炎症反应所触发的信号通路进行了表征。此外，我们将讨论AMD病理是否可能代表人类黄斑区固有免疫防御慢性激活的结果。
