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NEUROLOGY 2010;74:S17-S24
© 2010 American Academy of Neurology

Interferon-β mechanisms of action in multiple sclerosis

Suhayl Dhib-Jalbut, MD and Steven Marks

From the Department of Neurology (S.D.-J.), University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick, NJ; and Expert Medical Education (S.M.), Washington, DC.

Address correspondence and reprint requests to Dr. Suhayl Dhib-Jalbut, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Room 205, 97 Patterson Street, New Brunswick, NJ 08901-2160 jalbutsu{at}umdnj.edu

ABSTRACT Multiple sclerosis (MS) is a chronic autoimmune disease of the CNS characterized by inflammation, demyelination, and axonal injury. These pathologic effects are manifested in clinical symptoms of relapse and disability. Various disease-modifying therapies have been developed in recent years to modulate the body's immune response. Among the most widely used are the beta interferons (IFNβ). All produce comparable biological effects and are approved for the treatment of relapsing-remitting MS (RRMS). Although the precise mechanisms through which IFNβ achieves its antiinflammatory and immunomodulatory effects remain uncertain, several modes of action have been proposed, including inhibition of T-cell activation and proliferation; apoptosis of autoreactive T cells; induction of regulatory T cells; inhibition of leukocyte migration across the blood-brain barrier; cytokine modulation; and potential antiviral activity. Endogenously produced IFNβ in the injured brain is also now believed to contribute to mediation of antiinflammatory and regenerative effects. All these mechanisms are believed to underlie the therapeutic effect of IFNβ in the treatment of RRMS.

Abbreviations: APC = antigen-presenting cells; BAFF = B-cell-activating factor; BBB = blood-brain barrier; EAE = experimental autoimmune encephalitis; Gd = gadolinium; IFN = interferon; IFNAR = type 1 IFN receptor; IL = interleukin; MHC = major histocompatibility complex; MMP = matrix metalloproteinase; MS = multiple sclerosis; PBMC = peripheral blood mononuclear cells; PD1– = programmed death receptor 1-negative; RRMS = relapsing-remitting multiple sclerosis; SC = subcutaneous; SLE = systemic lupus erythematosus; sTNF-RII = soluble TNF-receptor II; sVCAM = soluble vascular cell adhesion molecule-1; TGF = transforming growth factor; Th = T helper; TIMP-1 = tissue inhibitor of MMP-type 1; TNF = tumor necrosis factor; Treg = T regulatory; TRIF = Toll-IL-1 receptor domain-containing adaptor inducing IFNβ; VLA-4 = very late antigen-4.

This supplement was supported by an educational grant from Teva Neuroscience. Expert Medical Education contributed to the editorial refinement of this article and to the production of this supplement. Authors may have accepted honoraria for their supplement contributions.

Disclosure: Author disclosures are provided at the end of the article.