Journal
ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY
Volume 1, Issue 8, Pages 622-631Publisher
WILEY-BLACKWELL
DOI: 10.1002/acn3.84
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Funding
- NCATS NIH HHS [UL1 TR000430] Funding Source: Medline
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Multiple sclerosis (MS) is a complex disorder of the central nervous system that appears to be driven by a shift in immune functioning toward excess inflammation that results in demyelination and axonal loss. Beta interferons were the first class of disease-modifying therapies to be approved for patients with MS after treatment with this type I interferon improved the course of MS on both clinical and radiological measures in clinical trials. The mechanism of action of interferon-beta appears to be driven by influencing the immune system at many levels, including antigen-presenting cells, T cells, and B cells. One effect of these interactions is to shift cytokine networks in favor of an anti-inflammatory effect. The pleiotropic mechanism of action may be a critical factor in determining the efficacy of interferon-beta in MS. This review will focus on select immunological mechanisms that are influenced by this type I cytokine.
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