Glatiramer acetate (GA; Copaxone; copolymer 1) exerts a clinical response in MS patients via its modulation of IFNγ and IL4 by reducing the expression of IFNγ and ensuring the stable expression of IL4 in anti-CD3/CD28stimulated peripheral blood mononuclear cells (PBMCs) [114] . Moreover, GA enhances the suppressive effects of Tregs in both EAE and MS [115, 116] . Studies of human DCs have shown that GA modulates the production of inflammatory mediators without affecting DC maturation or immunostimulatory potential. DCs exposed to GA secrete low levels of the Th1-polarizing factor IL12p70 in response to lipopolysaccharide and triggering of the CD40 ligand [117] . Human DCs exposed to GA also induce IL4-secreting effector Th2 cells and increase their expression of IL10 [118] . These results show that APCs, including DCs, are essential for the GA-mediated shift in Th-cell phenotypes and indicate that DCs are an important target of the immunomodulatory effects of GA.