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.
Bibliographical noteFunding Information:
This study was supported by a grant from Teva Pharmaceutical Industries (Israel), by a grant from the International Human Frontier Science Program Organization, and by a grant from the Israel Science Foundation (grant No. 812/08). N.F. is incumbent of the Pauline Recanati career development chair. We thank Dr. Ilan Volovitz for his help in the spinal cord cell isolation, Dr. Shlomit Reich-Zeliger for her help with multicolor FACS experiments, Dr. Yaron Antebi for help with FACS data analysis, Mrs. Veronique Amor for help in the IVIS experiments and Mrs. Haya Avital for the graphic work.
- Experimental autoimmune encephalomyelitis
- Glatiramer acetate
- Multiple sclerosis
- T-regulatory cells