To identify the mechanisms relevant for the therapeutic effect of glatiramer acetate (GA), we studied T- and B- regulatory cells as well as GM-CSF expression in mice recovered from experimental autoimmune encephalomyelitis (EAE). Selective depletion of Tregs reduced but did not eliminate the ability of GA to ameliorate EAE, indicating a role for additional immune-subsets. The prevalence of Bregs in the periphery and the CNS of EAE-mice increased following GA-treatment. Furthermore, GA downregulated the pathological expression of GM-CSF, on both the protein and mRNA levels. These findings corroborate the broad immunomodulatory mechanism of action of GA in EAE/MS.
- B-regulatory cells (Bregs)
- Experimental autoimmune encephalomyelitis
- Glatiramer acetate (GA)
- Granulocyte-macrophage colony-stimulating factor (GM-CSF)
- Multiple sclerosis
- T-regulatory cells (Tregs)