Multiple sclerosis (MS) is the most prevalent autoimmune disease affecting the
central nervous system (CNS). Its pathophysiology is centered on neuron myelin sheath destruction
in a manner largely dependent upon CD4+/CD8+ T-cell autoreactivity against myelin
antigens, inducing Th1/Th17 pathogenic responses with the resulting production of free
radicals and soluble mediators that exhibit the effector mechanisms of neurodegeneration.
The immune response responsible for this disease is complex and challenges modern medicine.
Consequently, many experimental therapies have been proposed in addition to the classical array of immunoregulatory/
immunosuppressive drugs that are normally used to treat MS. In this review, we will describe
the effects and mechanisms of action of widely used disease-modifying MS drugs as well as those of select
treatments that are currently in the experimental phase. Special emphasis is placed on helminth-derived immunoregulators,
as some of them have shown promising results. Additionally, we will compare the mechanisms
of action of both the MS drugs and the helminth-derived treatments to discuss the potential importance
of some signaling pathways in the control of MS.
Keywords: Multiple sclerosis, experimental autoimmune encephalomyelitis, helminths, antigens, glycans, immunoregulation.
Rights & PermissionsPrintExport