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Boosting lesion repair in multiple sclerosis by preventing lipid overload in phagocytes. (R-6832)

Macrophages are immune cells that are responsible for myelin breakdown in the brain of people with multiple sclerosis. However, macrophages also have beneficial properties and can contribute to repair of damaged sites in the brain. Our findings show that uptake of high amounts of myelin by macrophages induces lipid overload in these cells which impairs the beneficial properties. In this project we will elucidate the pathways involved in myelin induced lipid overload, and target these pathways to prevent this overload.
Date:1 Jan 2016  →  31 Dec 2017
Disciplines:Immunology, Laboratory medicine, Medical systems biology, Molecular and cell biology