Different Complement Activation Patterns Following C5 Cleavage in MOGAD and AQP4-IgG+NMOSD
Kimihiko Kaneko, Hiroshi Kuroda, Yuki Matsumoto, Naohiro Sakamoto, Naoya Yamazaki, Naoki Yamamoto, Shu Umezawa, Chihiro Namatame, Hirohiko Ono, Yoshiki Takai, T. Takahashi, Juichi Fujimori, Ichiro Nakashima, Yasuo Harigaya, Hans Lassmann, Kazuo Fujihara, Tatsuro Misu, Masashi Aoki
Abstract
OBJECTIVES: In myelin oligodendrocyte glycoprotein IgG-associated disease (MOGAD) and aquaporin-4 IgG+ neuromyelitis optica spectrum disorder (AQP4+NMOSD), the autoantibodies are mainly composed of IgG1, and complement-dependent cytotoxicity is a primary pathomechanism in AQP4+NMOSD. We aimed to evaluate the CSF complement activation in MOGAD. METHODS: CSF-C3a, CSF-C4a, CSF-C5a, and CSF-C5b-9 levels during the acute phase before treatment in patients with MOGAD (n = 12), AQP4+NMOSD (n = 11), multiple sclerosis (MS) (n = 5), and noninflammatory neurologic disease (n = 2) were measured. RESULTS: = 0.044). DISCUSSION: The complement pathway is activated in both MOGAD and AQP4+NMOSD, but MAC formation is lower in MOGAD, particularly in those with mild attacks, than in AQP4+NMOSD. These findings may have pathogenetic and therapeutic implications in MOGAD.