Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune, inflammatory astrocytopathy associated with anti-aquaporin-4 (AQP4) IgG antibodies. NMOSD is typically characterized by recurrent optic neuritis and longitudinal extensive transverse myelitis, although neurological involvement in other regions, such as the brain stem, hypothalamus and cerebral white matter, is known [ [1] Pereira W.L. Reiche E.M. Kallaur A.P. Kaimen-Maciel D.R. Epidemiological, clinical, and immunological characteristics of neuromyelitis optica: a review. ]. The primary target of immune attack in NMOSD is considered to be AQP4 on the cell surface of astrocytes. Anti-AQP4 IgG activates the complement cascade, and complement-dependent cytotoxicity and antibody-dependent cell-mediated cytotoxicity are considered the main pathophysiological mechanisms of astrocyte cytotoxicity in NMOSD [ [2] Misu T. Höftberger R. Fujihara K. Wimmer I. Takai Y. Nishiyama S. Nakashima I. Konno H. Bradl M. Garzuly F. Itoyama Y. Aoki M. Lassmann H. Presence of six different lesion types suggests diverse mechanisms of tissue injury in neuromyelitis optica. ]. In contrast, the presence of neutrophils is one of the characteristics of acute NMOSD lesions. However, its role is still unclear.