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Novel role for SLPI in MOG-induced EAE revealed by spinal cord expression analysis.
Mueller AM, Pedré X, Stempfl T, Kleiter I, Couillard-Despres S, Aigner L, Giegerich G, Steinbrecher A.
J Neuroinflammation. 2008 May 26;5:20.
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Temporal expression and cellular origin of CC chemokine receptors CCR1, CCR2 and CCR5 in the central nervous system: insight into mechanisms of MOG-induced EAE.
Eltayeb S, Berg AL, Lassmann H, Wallström E, Nilsson M, Olsson T, Ericsson-Dahlstrand A, Sunnemark D.
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Analysis of gene expression in MOG-induced experimental autoimmune encephalomyelitis after treatment with a novel brain-penetrating antioxidant.
Gilgun-Sherki Y, Barhum Y, Atlas D, Melamed E, Offen D.
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CX3CL1 (fractalkine) and CX3CR1 expression in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis: kinetics and cellular origin.
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Differential expression of protease M/neurosin in oligodendrocytes and their progenitors in an animal model of multiple sclerosis.
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Microglial and astroglial reactions to inflammatory lesions of experimental autoimmune encephalomyelitis in the rat central nervous system.
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Activity of a newly identified serine protease in CNS demyelination.
Scarisbrick IA, Blaber SI, Lucchinetti CF, Genain CP, Blaber M, Rodriguez M.
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Critical role of antigen-specific antibody in experimental autoimmune encephalomyelitis induced by recombinant myelin oligodendrocyte glycoprotein.
Lyons JA, Ramsbottom MJ, Cross AH.
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Sequential expression of transforming growth factor-beta1 by T-cells, macrophages, and microglia in rat spinal cord during autoimmune inflammation.
Kiefer R, Schweitzer T, Jung S, Toyka KV, Hartung HP.
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Gene-expression profiling of the early stages of MOG-induced EAE proves EAE-resistance as an active process.
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Congenic mapping confirms a locus on rat chromosome 10 conferring strong protection against myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis.
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Involvement of neuropsin in the pathogenesis of experimental autoimmune encephalomyelitis.
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Chronic relapsing experimental autoimmune encephalomyelitis with a delayed onset and an atypical clinical course, induced in PL/J mice by myelin oligodendrocyte glycoprotein (MOG)-derived peptide: preliminary analysis of MOG T cell epitopes.
Kerlero de Rosbo N, Mendel I, Ben-Nun A.
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The clinical course of experimental autoimmune encephalomyelitis is associated with a profound and sustained transcriptional activation of the genes encoding toll-like receptor 2 and CD14 in the mouse CNS.
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Increased calpain expression in activated glial and inflammatory cells in experimental allergic encephalomyelitis.
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Modulation of microglial/macrophage activation by macrophage inhibitory factor (TKP) or tuftsin (TKPR) attenuates the disease course of experimental autoimmune encephalomyelitis.
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