A serum autoantibody marker of neuromyelitis optica: distinction from multiple sclerosis.

By V. Lennon, D. Wingerchuk, T. Kryzer, S. Pittock, C. Lucchinetti, K. Fujihara, I. Nakashima, B. Weinshenker. The Lancet, 2004

3,129 citations recorded by the source corpus.

Subfields: Neurology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/a3e10a940c1042ea3ea156a8b4903034a5e31a6c

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Citations in the corpus

Aquaporin water channels in the nervous system (2013, neutral): “It was thought to be a variant of multiple sclerosis (MS) until 2004, when serum antibodies against a perivascular brain antigen were detected in individuals with NMO but not in patients with MS 112 ; these antibodies were subsequently shown to be against AQP4 (REF.”
MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis (2009, background): “Upregulation of miR-326 was associated only with multiple sclerosis, as patients with NMO, another CNS inflammatory disorder similar to multiple sclerosis but mediated by antoantibodies, showed no miR-326 upregulation in PBL”
Neuromyelitis optica brain lesions localized at sites of high aquaporin 4 expression. (2006, background): “The serum autoantibody NMO-IgG was reported as a biomarker of NMO in 2004.(2) It is detected by indirect immunofluorescence assay on a substrate of mouse CNS tissue.”
Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: A multicentre study of 175 patients (2012, background): “NMO is associated with serum antibodies to aquaporin4, the most abundant water channel in the CNS in up to 80% of cases [2-7].”
Pattern-specific loss of aquaporin-4 immunoreactivity distinguishes neuromyelitis optica from multiple sclerosis. (2007, background): “Lennon et al. subsequently identified a specific marker autoantibody (NMO-IgG), which interacts selectively with the AQP4 water channel (Lennon et al., 2005).”
MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses, and long-term outcome (2016, background): “5 months since onset, median 52 [1-507] months), the disease took a relapsing course in most cases.”
The Immunopathology of Multiple Sclerosis: An Overview (2007, background): “Autoantibodies against Aquaporin 4 have recently been identified as a specific serological marker in patients with either Devic’s disease or patients with isolated longitudinally extensive myelitis (54, 55, 91).”
Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research. (2006, background): “…generation of myelin-specific antibodies by B lymphocytes, and the same mechanism appears to be involved in the pathogenesis of lesion formation in both a subset of multiple sclerosis patients (Lucchinetti et al., 2000) and patients with Devic's type of neuromyelitis optica (Lennon et al., 2004).”
Anti-aquaporin-4 antibody is involved in the pathogenesis of NMO: a study on antibody titre. (2007, methodology): “Recently, its disease-specific serum autoantibody, NMO-IgG, was discovered in an indirect immunofluorescence method (Lennon et al., 2004), and based on a study of the sera of 13 patients with high titres of NMO-IgG, its target antigen was identified as aquaporin-4 (AQP4) water channel protein mainly”