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Boosting lesion repair in multiple sclerosis by preventing lipid overload in phagocytes / Short title: Fatty acids control foamy phagocyte function (R-9694)
Multiple sclerosis (MS) is a neurodegenerative autoimmune disease of the central nervous system in which phagocytes play a crucial role. Myelin-containing phagocytes are the most abundant cell type in MS lesions and display a transient wound-healing phenotype. To date, the hubs and drivers of this phenotype remain poorly understood. Our data indicate that prolonged intracellular myelin accumulation disturbs the wound-healing phenotype of phagocytes. Furthermore, our data show that enzymes involved in fatty acid metabolism underlie this phenotype shift. In this study, we validate and elaborate on the role of these enzymes in driving the phenotype of phagocytes in MS patients.
Date:1 Jan 2019 → 31 Dec 2020
Keywords:AUTOIMMUNE DISEASES, central nervous system, MULTIPLE SCLEROSIS
Disciplines:Inflammation, Neurological and neuromuscular diseases