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Astrocytes play a key role in EAE pathophysiology by orchestrating in the CNS the inflammatory response of resident and peripheral immune cells and by suppressing remyelination

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Osteopontin is upregulated during in vivo demyelination and remyelination and enhances myelin formation in vitro

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Panglial Gap Junctional Communication is Essential for Maintenance of Myelin in the CNS

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Chondroitin sulfate proteoglycans inhibit oligodendrocyte myelination through PTPσ

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Altered expression of glutamate transporters in experimental autoimmune encephalomyelitis

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Cdc42 and Rac1 Signaling Are Both Required for and Act Synergistically in the Correct Formation of Myelin Sheaths in the CNS

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Astrocyte TNFR2 is required for CXCL12-mediated regulation of oligodendrocyte progenitor proliferation and differentiation within the adult CNS

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Tumor Necrosis Factor α Mediates Lipopolysaccharide-Induced Microglial Toxicity to Developing Oligodendrocytes When Astrocytes Are Present

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Astrocytic Tissue Inhibitor of Metalloproteinase-1 (TIMP-1) Promotes Oligodendrocyte Differentiation and Enhances CNS Myelination

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IFNβ secreted by microglia mediates clearance of myelin debris in CNS autoimmunity

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CNS-specific Therapy for Ongoing EAE by Silencing IL-17 Pathway in Astrocytes

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