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Research Article| Volume 333, ISSUE 1-2, P55-59, October 15, 2013

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Origins and significance of astrogliosis in the multiple sclerosis model, MOG peptide EAE

  • Monica Moreno
    Affiliations
    Institute for Pediatric Regenerative Research, UC Davis School of Medicine and Shriners Hospitals for Children Northern California, United States
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  • Fuzheng Guo
    Affiliations
    Institute for Pediatric Regenerative Research, UC Davis School of Medicine and Shriners Hospitals for Children Northern California, United States
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  • Emily Mills Ko
    Affiliations
    Institute for Pediatric Regenerative Research, UC Davis School of Medicine and Shriners Hospitals for Children Northern California, United States
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  • Peter Bannerman
    Affiliations
    Institute for Pediatric Regenerative Research, UC Davis School of Medicine and Shriners Hospitals for Children Northern California, United States
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  • Athena Soulika
    Affiliations
    Institute for Pediatric Regenerative Research, UC Davis School of Medicine and Shriners Hospitals for Children Northern California, United States
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  • David Pleasure
    Correspondence
    Corresponding author at: UC Davis School of Medicine, c/o Shriners Hospital, 2425 Stockton Blvd, Sacramento CA 95817, United States, Fax: +1 916 453 2288.
    Affiliations
    Institute for Pediatric Regenerative Research, UC Davis School of Medicine and Shriners Hospitals for Children Northern California, United States
    Search for articles by this author
Published:January 07, 2013DOI:https://doi.org/10.1016/j.jns.2012.12.014

      Abstract

      Astroglia, the most abundant cells in the human CNS, and even more prominent in multiple sclerosis patients, participate in CNS innate and adaptive immunity, and have been hypothesized to play an important role in multiple sclerosis progression. Experimental autoimmune encephalomyelitis elicited in mice by immunization with myelin oligodendrocyte glycoprotein peptide 35–55 provides a means by which to explore the genesis and disease significance of astrogliosis during a chronic immune-mediated CNS inflammatory/demyelinative disorder that, in its' pathological features, strongly resembles multiple sclerosis.

      Keywords

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