Figure 1.

Anti-inflammatory mechanisms induced by glatiramer acetate (GA). GA treatment on antigen-presenting cells (APCs) leads to anti-inflammatory differentiation. Treatment modulates innate stimuli and is associated with down-regulation of type I interferon (IFN), increased T helper (Th)2, and regulatory T (Treg) cell differentiation. Reactivation of GA-reactive Th2 cells in periphery through presentation of myelin antigens is associated with bystander suppression. Th2 cells also modulate B-cell activation. Treg cells down-regulate secretion of proinflammatory cytokines by effector T (Teff) cells both in periphery and in the central nervous system (CNS). CD8⁺ T cells are generated by antigen presentation of GA in periphery and migrate to the CNS where they contribute to inhibiting myelin degradation. IL, Interleukin; TNF, tumor necrosis factor; IFNAR, interferon-receptor; MHC, major histocompatibility complex; BDNF, brain-derived neurotrophic factor; IGF, insulin-like growth factor; IDO, indoleamine-2,3-dioxygenase; solid lines, cytokines produced by the representative cells; dashed lines, reduced production of cytokines; red lines: inhibitory cytokines.