Immune Mechanisms in Retinal Degeneration

Karlstetter, M. and Langmann, T. (2012) Immune Mechanisms in Retinal Degeneration. KLINISCHE MONATSBLATTER FUR AUGENHEILKUNDE, 229 (3). pp. 221-226. ISSN 0023-2165, 1439-3999

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Abstract

Hereditary retinal dystrophies are characterised by a common apoptotic pathway leading to progressive retinal degeneration. Similar degenerative processes are evident in multifactorial and complex retinal disorders including age-related macular degeneration. To understand early triggers of these mechanisms, genetic and experimental mouse models have been developed that mimic various forms of human retinal degeneration. In most of these models, early chronic activation of the innate immune system has been documented. This process mainly involves the complement cascade as humoral component and microglial cells as sensors and effectors of the retinal immune response. Current evidence suggests that the genetic predisposition and individual factors like age or diet critically influence the immune homeostasis in the retina. Based on their effectiveness, innate immune mechanisms are thought to support or even provoke retinal degeneration. This review article summarises recent progress in understanding the role of innate immunity in retinal degenerative diseases. We especially focus on human studies and attempt to provide a link between activation of the complement system and microglial function. Moreover, concepts are presented that highlight the retinal immunopathology as potential therapeutic target to prevent vision loss.

Item Type: Article
Uncontrolled Keywords: FACTOR-H POLYMORPHISM; MACULAR DEGENERATION; RETINITIS-PIGMENTOSA; ACTIVATED MICROGLIA; PHOTORECEPTOR DEGENERATION; COMPLEMENT ACTIVATION; APOPTOTIC CELLS; MOUSE RETINA; RCS RAT; DYSTROPHY; genetics; retina; microglia; complement system; retinal degeneration
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Humangenetik
Depositing User: Petra Gürster
Date Deposited: 11 May 2020 06:45
Last Modified: 11 May 2020 06:45
URI: https://pred.uni-regensburg.de/id/eprint/19154

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