Lipid overload blunts the reparative properties of phagocytes in MS lesions (R-8638)

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 recent data indicate that prolonged intracellular myelin accumulation disturbs the wound- healing phenotype of myelin-containing phagocytes. Furthermore, our data show that an enzyme involved in fatty acid metabolism underlies this inflammatory phenotype shift. Importantly, animals lacking this enzyme demonstrate reduced neuroinflammation and enhanced CNS repair in in vivo models. In this study, we validate and elaborate on the role of this enzyme in driving the phenotype of phagocytes and how absence of this enzyme impact CNS repair and neuroinflammation.

Keywords:MULTIPLE SCLEROSIS

Disciplines:Immunology