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Although TNF antagonists are efficacious in treating a range of autoimmune conditions, they exacerbate or even promote multiple sclerosis (MS)--a clinical finding that has been a conundrum for over a decade and has been a source of debate regarding the role of these drugs and of TNF signaling in the development of demyelinating disease. Recent work investigating the functional consequences of MS-associated genetic variation in the gene encoding TNFR1 has demonstrated that genetic risk drives the production of a novel, endogenous TNF antagonist. This mirrors the clinical experience with the drugs and indicates that the net effect of TNF function in MS development is a protective one, warranting a re-evaluation of the studies that have contributed to our understanding of TNF signaling in inflammation, immunoregulation and neuroprotection, to determine how future research can be directed towards targeting this pathway for therapeutic benefit.

Original publication

DOI

10.2217/pgs.13.140

Type

Journal article

Journal

Pharmacogenomics

Publication Date

09/2013

Volume

14

Pages

1397 - 1404

Keywords

Genome-Wide Association Study, Humans, Inflammation, Molecular Targeted Therapy, Multiple Sclerosis, Receptors, Tumor Necrosis Factor, Type I, Signal Transduction, Tumor Necrosis Factor-alpha