2026 Volume 43 Issue 3 Pages 227-230
Neuromyelitis optica spectrum disorder (NMOSD) is characterized by ‘autoimmune aquaporin–4 (AQP4)–opathy’. Damages of AQP4–expressing glial cells (e.g., astrocytes) would be caused by (a) complement–dependent cytotoxicity (CDC), (b) antibody–dependent cytotoxicity (ADCC), and (c) internalization of AQP4 water channels in NMOSD. Recent research advances reveal that stage–dependent immune dynamics, composed of neutrophils, TH17 cells, Treg cells, and TRM cells, can modify the pathogenesis of NMOSD in situ. Therefore, modification of these immune dynamics could yield future drug candidates for NMOSD, in addition to complement–depleting antibodies, anti–interleukin–6 receptor antibodies, and B–cell–depleting antibodies. We would provide suggestions for establishing predictive biomarkers of disease activities and treatment responses, and for developing treatment strategies for NMOSD, to advance precision medicine for NMOSD.
