Abstract
Background: Multiple sclerosis (MS) is considered a disease with an immunopathogenesis that is distinct from neuromyelitis optica spectrum disorders (NMOSD). In NMOSD, plasmablasts (PB) were anti-AQP4 antibody-producing cells, and the IL-6 receptor (IL-6R) signaling pathway was crucial for their survival (Chihara, PNAS 2011). We previously described the clinical efficacy of tocilizumab (TCZ), a humanized anti-IL-6R monoclonal antibody, in patients with anti-AQP4 antibody positive NMOSD (Araki, Neurology 2014). However, the interferon-β non-responders, but not the responders with MS, tended to have a higher PB frequency.
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