Relationship Between NMO-Antibody and Anti–MOG Antibody in Optic Neuritis

  title={Relationship Between NMO-Antibody and Anti–MOG Antibody in Optic Neuritis},
  author={Takeshi Kezuka and Yoshihiko Usui and Naoyuki Yamakawa and Yoshimichi Matsunaga and Ryusaku Matsuda and Masayuki Masuda and Hiroya Utsumi and Keiko Tanaka and Hiroshi Goto},
  journal={Journal of Neuro-Ophthalmology},
Background: Damage to astrocytes by anti-aquaporin-4 antibody (AQP4-Ab), also known as NMO antibody, has been implicated as the cause of neuromyelitis optica. Myelin oligodendrocyte glycoprotein (MOG) is well known as the causative protein of multiple sclerosis (MS). MOG antigen is currently considered as a cause of optic neuritis (ON) associated with MS because immunization with MOG antigen derived from oligodendrocytes induces murine ON with myelitis. We investigated the relationship between… 

Clinical Profile of Anti-Myelin Oligodendrocyte Glycoprotein Antibody Seropositive Cases of Optic Neuritis

MOG-Abs may contribute to the heterogeneous clinical picture of optic neuritis, and although visual acuity outcome is favourable, there is a tendency of residual visual field deficit and a possibility of repeated relapses.

Antibodies to myelin oligodendrocyte glycoprotein in bilateral and recurrent optic neuritis

MOG antibodies have a strong association with BON and may be a useful clinical biomarker, and Class II evidence that MOG antibodies are associated with AQP4 antibody–negative BON is provided.

Glycine receptor and myelin oligodendrocyte glycoprotein antibodies in Turkish patients with neuromyelitis optica

Distinction between MOG antibody-positive and AQP4 antibody-positive NMO spectrum disorders

Patients with NMOSD with MOG antibodies have distinct clinical features, fewer attacks, and better recovery than patients with AQP4 antibodies or patients seronegative for both antibodies.

Myelin oligodendrocyte glycoprotein antibodies in neurological disease

Antibodies against myelin oligodendrocyte glycoprotein (MOG-Abs) that are detectable with cell-based assays are associated with non-MS acquired demyelinating syndromes of the CNS, including the value of detection assays and evidence for antibody pathogenicity and its mechanism.

Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype

MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO and MS with an opticospinal presentation, and anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype.

MOG cell-based assay detects non-MS patients with inflammatory neurologic disease

This study provides Class II evidence that the presence of serum IgG1- MOG-Abs in AQP4-Ab–negative patients distinguishes non-MS CNS demyelinating disorders from MS (sensitivity 24, 95% confidence interval [CI] 9%–45%; specificity 100%, 95% CI 88%–100%).

Antibodies to myelin oligodendrocyte glycoprotein in idiopathic optic neuritis

Although not proving primary pathogenicity of anti-MOG antibodies, the present results indicate that the measurement of MOG antibodies is useful in diagnosing and treating ON.



Antibody to aquaporin-4 in the long-term course of neuromyelitis optica

A strong relationship between AQP4-Abs and clinical state is demonstrated, and the hypothesis that these antibodies are involved in the pathogenesis of NMO is supported.

Neuromyelitis optica pathogenesis and aquaporin 4

Dysregulation of tolerance associated with autoimmune disease appears to have a role in NMO and reagents and experimental questions that need to be developed and addressed are identified to enhance the understanding of the pathogenesis of NMO.

Pathogenic potential of IgG binding to water channel extracellular domain in neuromyelitis optica

NMO patients’ serum IgG has a selective pathologic effect on cell membranes expressing aquaporin-4, and targeting astrocytic processes around nodes of Ranvier could initiate demyelination.

Anti-aquaporin 4 antibody in selected Japanese multiple sclerosis patients with long spinal cord lesions

It is suggested that Japanese OSMS with LCL may have an underlying pathogenesis in common with NMO, and an immunohistochemical detection system for the anti-AQP4 antibodies is established using the AQP4-transfected human embryonic kidney cell line.

IgG marker of optic-spinal multiple sclerosis binds to the aquaporin-4 water channel

It is shown that NMO-IgG binds selectively to the aquaporin-4 water channel, a component of the dystroglycan protein complex located in astrocytic foot processes at the blood-brain barrier, which may represent the first example of a novel class of autoimmune channelopathy.

Neuromyelitis optica and non organ-specific autoimmunity.

Neuromyelitis optica spectrum disorders with seropositive findings for NMO-IgG occurring with SS/SLE or non-organ-specific autoantibodies is an indication of coexisting NMO rather than a vasculopathic or other complication of SS/ SLE.

Anti-myelin antibodies do not allow earlier diagnosis of multiple sclerosis

There was no evidence that the MS status based on either the McDonald or Poser criteria relates to the antibody status.

Pathogenic myelin oligodendrocyte glycoprotein antibodies recognize glycosylated epitopes and perturb oligodendrocyte physiology.

It is demonstrated that pathogenic and nonpathogenic anti-MOG antibodies have a consistent array of differences in their recognition of antigenic determinants and biological effects, and in vitro tools for determining autoimmune antibody pathogenicity in multiple sclerosis patients are suggested.

Immune Responses Against the Myelin/Oligodendrocyte Glycoprotein in Experimental Autoimmune Demyelination

Experimental data currently available on specificity and pathogenic roles of T cell and antibody responses against MOG are reviewed, which have implications relevant to multiple sclerosis and related disorders.

Frontline: Epitope recognition on the myelin/oligodendrocyte glycoprotein differentially influences disease phenotype and antibody effector functions in autoimmune demyelination

It is provided proof that in marmoset EAE, autoantibodies reactive against conformational epitopes of MOG are not only responsible for aggravating demyelination, but also an essential factor for disease dissemination in space within the central nervous system, a hallmark for typicalforms of human MS.