Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6021089 | Journal of Neuroimmunology | 2011 | 12 Pages |
Abstract
The C57Bl/6 mouse is the preferred host for the maintenance of gene deletion mutants and holds a unique place in investigations of cytokine/chemokine networks in neuroinflammation. It is also susceptible to experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis (MS)-like disease commonly used to assess potential MS therapies. Investigations of glial reactivity in EAE have revealed hitherto undescribed astroglial responses in this model, characterized by progressively diminishing glial fibrillary acidic protein and aquaporin-4 immunostaining, from early disease. These observations show that astrocyte responses vary with the EAE paradigm and are an important pathological criterion for disease mapping and therapy evaluation.
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Authors
Hong Pham, Juliane Doerrbecker, Anton A. Ramp, Claretta S. D'Souza, Dhana G. Gorasia, Anthony W. Purcell, Margaret M. Ayers, Jacqueline M. Orian,