Differential mechanisms of action of interferon-beta and glatiramer aetate in MS

Abstract

Interferon-beta and glatiramer acetate (GA) are the two main groups of drugs used in the treatment of MS. Notably, while both ultimately decrease CNS inflammation, they do so by very different mechanisms. Interferon-beta has potent activity at the blood-brain barrier and impairs the trafficking of inflammatory cells into the CNS. In contrast, GA has negligible effect at the blood-brain barrier, allowing GA-specific T helper 2 lymphocytes to enter the CNS to decrease inflammation through bystander suppression. Other differences are also emphasized. The presence of GA-reactive lymphocytes within the CNS parenchyma may have the additional benefit of conferring neuroprotection through protective autoimmunity.