視神経脊髄炎に対するIL–6R抗体治療：現状と課題

抄録

Neuromyelitis optica (NMO) is an inflammatory disease that resembles MS in the relapsing clinical course and occurrence of optic neuritis and myelitis. Two decades of studies have revealed that the antibody, reactive to a water channel protein AQP4, induces inflammatory pathology of NMO, which is mediated by proinflammatory cytokines, chemokines, and various inflammatory cells. The presumed disease mechanism constructed based on accumulating studies has led to the identification of possible targets of therapy, including interleukin–6 (IL–6) receptor signaling. Our group has discovered the role of IL–6R signaling in the pathomechanism of NMO, and showed the potential efficacy of anti–IL–6R antibody tocilizumab in NMO patients. Remarkably, recent randomized controlled clinical trials have shown the therapeutic efficacy of antibodies specific for IL–6 receptor satralizumab in the core patients of NMO, although there is no evidence for the efficacy in anti–AQP4 antibody–negative patients. The results imply that anti–AQP4 antibody is a biomarker predicting the efficacy of therapies, and indicate the future direction towards “precision medicine”. Given that the development of anti–IL–6R therapy was driven by academia and translational scientists in Japan, it is time to consider how to maintain and develop this construct for the future.