Neuromyelitis optica (NMO), also known as Devic’s disease, is a central nervous system (CNS) autoimmune disease that preferentially affects the spinal cord and optic nerve. The disease is mediated by autoantibodies against aquaporin 4 (AQP4). Myasthenia gravis (MG) is a well-recognized disease affecting the neuromuscular junction, mediated by autoantibodies against the acetylcholine receptor (AChR). Recent studies have reported an increased prevalence of NMO in patients with MG. To verify whether coexisting autoimmune disease may exacerbate experimental autoimmune MG, the present study investigated whether active immunization with AQP4 peptides or passive transfer of NMO-Ig can affect the severity of experimental autoimmune MG (EAMG). Injection of either AQP4 peptide or NMO-Ig to EAMG or to naive mice caused increased fatigability and aggravation of EAMG symptoms as expressed by augmented muscle weakness (but not paralysis), decremental response to repetitive nerve stimulation, increased neuromuscular jitter, and aberration of immune responses. Thus, our study shows increased disease severity in EAMG mice following immunization with the NMO autoantigen AQP4 or by NMO-Ig, mediated by augmented inflammatory response.
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Mizrachi T, Brill L, Rabie M, et al. NMO-IgG and AQP4 Peptide Can Induce Aggravation of
EAMG and Immune-Mediated Muscle Weakness. J Immunol Res. 2018 May 22;2018:5389282.
