Age-related macular degeneration: activation of innate immunity system via pattern recognition receptors.
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.
Kaarniranta
K
K
Department of Ophthalmology, Institute of Clinical Medicine, University of Kuopio, P.O. Box 1627, 70211, Kuopio, Finland. kai.kaarniranta@uku.fi
Salminen
A
A
D000818:Animals; D017242:Complement Factor H / Q000235:genetics; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology*; D008268:Macular Degeneration / Q000235:genetics / Q000276:immunology / Q000503:physiopathology*; D008954:Models, Biological; D011110:Polymorphism, Genetic; D051192:Receptors, Pattern Recognition / Q000502:physiology*; D051193:Toll-Like Receptors / Q000502:physiology
D051192:Receptors, Pattern Recognition; D051193:Toll-Like Receptors; D017242:Complement Factor H