Symposien Donnerstag

Änderungen im Programmablauf vorbehalten.

 
engl
Raum Paris 08:00 - 09:30 01.10.2015
Symposium Do05
Microglia as target for retinal therapy
Vorsitzende/r: Thomas Langmann (Köln), Solon Thanos (Münster)

Resident microglial cells can be regarded as the immunological watchdogs of the retina. There is strong evidence from animal models and in situ analyses of human tissue that microglial reactivity is a common hallmark of various retinal degenerative and inflammatory diseases. These include rare hereditary retinopathies but also comprise more common multifactorial retinal diseases such as age-related macular degeneration, diabetic retinopathy, glaucoma, and uveitis as well as neurological disorders with ocular manifestation. In this session we present the concept that this resident immune cell of the retina cannot be simply regarded as bystander of disease but may instead be a potential therapeutic target to be modulated in the treatment of degenerative and inflammatory diseases of the retina.
Referent/in: Marta Agudo-Barriuso (Murcia)
Upon unilateral axonal injury, retinal ganglion cells (RGC) in the injured retina die. Their bodies are engulfed by phagocytic microglial cells (PMC) whose number and topography parallel the course of RGC death. In the contralateral uninjured retina there is a PMC response that occurs independently of course and rate of RGC death in the injured retina.
Referent/in: Peter Hammes (Mannheim)
Referent/in: Rebecca Scholz (Köln)
Microglia activation is a common hallmark of retinal degenerative diseases. Our previous work showed that TSPO is a marker for reactive retinal microglia and that the TSPO ligand XBD173 exerts strong anti-inflammatory effects on microglia in vitro. Here we show that XBD173 treatment of mice challenged with withe light reduced the number of reactive microglia and protected the retina from light induced apoptosis. We conclude that TSPO represents a promising therapeutic target for retinal degenerations.
Referent/in: Francine Behar-Cohen (Lausanne)
Anti-VEGF drugs used in treating retinal diseases aim at controlling angiogenic processes and/or vascular leakage that are partly VEGF-driven. Sub-clinical inflammation is suspected to contribute to diabetic retinopathy and AMD pathogenesis but the effect of anti-VEGF on microglia in a non-angiogenic context, was not yet assessed. Using a rat model with acute intraocular inflammation, we showed that anti-VEGF injections, although not influencing the severity of inflammation, induced inhibitory effects on retinal and choroidal microglia activation.
Referent/in: Alexa Klettner (Kiel)
The retinal pigment epithelium (RPE) resides at the interface between retina and choroid, and is involved in the upkeep of the retinal immune privilege. It detects danger signals via pattern recognition receptors, such as Toll-like receptor (TLR)3 and can regulate the immune response of cells of the innate immune system, e.g. of retinal microglia. TLR3-activated RPE cells influence the response of the microglia in fine-tuned way, exacerbating the pro-inflammatory response without enhancing neurotoxic factors.
Referent/in: Solon Thanos (Münster)
Injury to the optic nerve, caused mechanically or by diseases, are still not reparable and result in retrograde and anterograde atrophy. A strategy to support regeneration may be the pharmacological alteration of microglial cells. The object of this work was to inactivate microglial cells, to support ganglion cell survival and to enhance the number of RGCs regenerating axons in vivo.