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- W2168436315 endingPage "662" @default.
- W2168436315 startingPage "651" @default.
- W2168436315 abstract "Multiple sclerosis (MS) is the prototypical inflammatory disease of the central nervous system (CNS). MS lesions harbor different immune cells, but the contribution of individual cell types to disease etiology and progression is not well understood. In experimental autoimmune encephalomyelitis (EAE), auto-reactive helper T (Th) cells instigate CNS inflammation by acting on myeloid cells via the production of granulocyte-macrophage colony-stimulating factor (GM-CSF). Recent reports have implicated myeloid cells in both the inflammatory process and as executers of tissue damage in the CNS. We review these findings here, and integrate them into a model wherein GM-CSF produced by Th cells coordinates monocyte recruitment to the CNS, and differentiation into pathogenic effectors. We discuss the implications of this model to current therapies for MS, and outline important areas of further inquiry." @default.
- W2168436315 created "2016-06-24" @default.
- W2168436315 creator A5014165093 @default.
- W2168436315 creator A5051595544 @default.
- W2168436315 creator A5072801840 @default.
- W2168436315 date "2015-10-01" @default.
- W2168436315 modified "2023-10-14" @default.
- W2168436315 title "GM-CSF in Neuroinflammation: Licensing Myeloid Cells for Tissue Damage" @default.
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