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Over the past three decades much has been elucidated about the pathogenesis and clinical manifestations of Guillain-Barré syndrome, the most common cause of acute flaccid paralysis worldwide. Cross-reactivity between surface epitopes on the bacterium Campylobacter jejuni and peripheral nerve gangliosides has been shown to induce antibody-mediated axonal-type neuropathy in some patients. Understanding the molecular mechanisms that cause nerve damage in these patients has led to the development of novel therapies, which specifically target the complement cascade and prevent formation of the membrane attack complex. The most promising, eculizumab, is a humanized monoclonal antibody, which blocks formation of human C5a and C5b-9, and has been shown to prevent antiganglioside antibody-induced neuropathy in vitro and in a mouse model and is currently in Phase II clinical trials.

Original publication

DOI

10.1586/14737175.2015.1065732

Type

Journal article

Journal

Expert Rev Neurother

Publication Date

2015

Volume

15

Pages

847 - 849

Keywords

Guillain–Barré syndrome, anti-ganglioside antibodies, complement cascade, miller fisher syndrome, molecular mimicry, Guillain-Barre Syndrome, Humans