GLIAL CELLSAstrocytic necrosis is induced by anti-aquaporin-4 antibody-positive serumKinoshita, Makotoa; Nakatsuji, Yujia; Moriya, Masayukia; Okuno, Tatsusadab; Kumanogoh, Atsushib; Nakano, Misac; Takahashi, Toshiyukid; Fujihara, Kazuoe; Tanaka, Keikof; Sakoda, SaburoaAuthor Information aDepartments of Neurology, Osaka University Graduate School of Medicine bImmunopathology, Research Institute for Microbial Diseases, Osaka University cDepartment of Neurology, Toyonaka Municipal Hospital, Osaka dDepartments of Neurology eMultiple Sclerosis Therapeutics, Tohoku University Graduate School of Medicine, Sendai fDepartment of Neurology, Kanazawa Medical University, Ishikawa, Japan Correspondence to Associate Professor Yuji Nakatsuji, MD, PhD, Department of Neurology, Osaka University, Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan Tel: +81 6 6879 3571; fax: +81 6 6879 3579; e-mail: [email protected] Received 24 September 2008 accepted 8 October 2008 NeuroReport: March 25, 2009 - Volume 20 - Issue 5 - p 508-512 doi: 10.1097/WNR.0b013e32832776f4 Buy Metrics Abstract Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of the central nervous system, and humoral immunity is suggested to play an important role in the pathogenesis. The identification of an anti-aquaporin-4 antibody (AQP4-Ab, neuromyelitis optica immunoglobulin G) in the sera of patients with NMO has led to the investigation on the pathogenicity of the autoantibody. Recent immunohistological analyses revealed the primary loss of AQP4 on astrocytes and complement deposition in active lesions of NMO. In this report, we show that astrocytes are susceptible to sera from AQP4-Ab-positive patients and undergo necrosis in a complement-dependent manner. Our results suggest the primary pathogenic role of AQP4-Ab in NMO. © 2009 Lippincott Williams & Wilkins, Inc.