Abstract

Despite the differences between multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE), most of the knowledge on immune-mediated tissue damage in MS is based on data from EAE. Immune response– modifying therapies such as TNFα inhibitors, glatiramer acetate (GA) or natalizumab have been studied in rodents and have been translated into treatment for patients with varying success. In humans treatment with an anti TNF monoclonal antibody or a recombinant TNF receptor Ig fusion protein resulted in enhanced inflammation. In contrast, findings from GA or natalizumab have been successful in human translation. Findings of EAE studies should be interpreted carefully and should be confirmed using substances (proof of principle). Only if successful, these substances should be studied in humans.

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