Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3064746 | Journal of Neuroimmunology | 2010 | 12 Pages |
Abstract
The aim of this study was to identify cell populations relevant to pathogenesis and repair within the injured CNS in mice that recovered from experimental autoimmune encephalomyelitis (EAE). We demonstrate that in two EAE models, with either relapsing–remitting or chronic course, T-cells and resident activated microglia manifested extensive IL-17 expression, with apparent localization within regions of myelin loss. In mice treated with glatiramer acetate (GA, Copaxone®), even when treatment started after disease exacerbation, CNS inflammation and Th-17 occurrence were drastically reduced, with parallel elevation in T-regulatory cells, indicating the immunomodulatory therapeutic consequences of GA treatment in situ.
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Authors
Rina Aharoni, Raya Eilam, Ariel Stock, Anya Vainshtein, Elias Shezen, Hilah Gal, Nir Friedman, Ruth Arnon,