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Abstract
CD4(+)CD25(+) regulatory T cells (Tregs) are potent immunosuppressors that are pivotal
in the maintenance of self-tolerance. The involvement of Tregs in therapies for immune-mediated
diseases has been proposed, but direct supporting evidence is still lacking. While
investigating mechanisms underlying the clinical benefits of glatiramer acetate (GA)
in an animal model of multiple sclerosis (MS), i.e., experimental autoimmune encephalomyelitis
(EAE), we recently demonstrated that GA can protect mice deficient in the Th(2) cytokines
IL-4, IL-10 and IL-4/IL-10 from acquiring EAE, suggesting that mechanisms other than
Th(2) cells may be responsible for the therapeutic effects of GA. Here we demonstrate
that GA treatment boosts the expression of Foxp3 on Tregs during EAE. Furthermore,
adoptive transfer of purified Tregs from GA-treated EAE mice is more effective in
preventing EAE development than Tregs from untreated EAE controls. Thus, our current
data provide evidence that Tregs may be the major contributor to GA's therapeutic
action in EAE and, possibly, MS. Further mechanistic studies to reveal the molecular
events linking GA with Tregs may optimize GA treatment and lead to the development
of new, even more effective therapies that utilize this mechanism of action.