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Title[redir]:
MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 1: Frequency, syndrome specificity, influence of disease activity, long-term course, association with AQP4-IgG, and origin | Journal of Neuroinflammation | Full Text
Description:
Background Antibodies to myelin oligodendrocyte glycoprotein (MOG-IgG) have been suggested to play a role in a subset of patients with neuromyelitis optica and related disorders. Objective To assess (i) the frequency of MOG-IgG in a large and predominantly Caucasian cohort of patients with optic neuritis (ON) and/or myelitis; (ii) the frequency of MOG-IgG among AQP4-IgG-positive patients and vice versa; (iii) the origin and frequency of MOG-IgG in the cerebrospinal fluid (CSF); (iv) the presence of MOG-IgG at disease onset; and (v) the influence of disease activity and treatment status on MOG-IgG titers. Methods 614 serum samples from patients with ON and/or myelitis and from controls, including 92 follow-up samples from 55 subjects, and 18 CSF samples were tested for MOG-IgG using a live cell-based assay (CBA) employing full-length human MOG-transfected HEK293A cells. Results MOG-IgG was detected in 95 sera from 50 patients with ON and/or myelitis, including 22/54 (40.7%) patients with a history of both ON and myelitis, 22/103 (21.4%) with a history of ON but no myelitis and 6/45 (13.3%) with a history of longitudinally extensive transverse myelitis but no ON, and in 1 control patient with encephalitis and a connective tissue disorder, all of whom were negative for AQP4-IgG. MOG-IgG was absent in 221 further controls, including 83 patients with AQP4-IgG-seropositive neuromyelitis optica spectrum disorders and 85 with multiple sclerosis (MS). MOG-IgG was found in 12/18 (67%) CSF samples from MOG-IgG-seropositive patients; the MOG-IgG-specific antibody index was negative in all cases, indicating a predominantly peripheral origin of CSF MOG-IgG. Serum and CSF MOG-IgG belonged to the complement-activating IgG1 subclass. MOG-IgG was present already at disease onset. The antibodies remained detectable in 40/45 (89%) follow-up samples obtained over a median period of 16.5 months (range 0–123). Serum titers were higher during attacks than during remission (p < 0.0001), highest during attacks of simultaneous myelitis and ON, lowest during acute isolated ON, and declined following treatment. Conclusions To date, this is the largest cohort studied for IgG to human full-length MOG by means of an up-to-date CBA. MOG-IgG is present in a substantial subset of patients with ON and/or myelitis, but not in classical MS. Co-existence of MOG-IgG and AQP4-IgG is highly uncommon. CSF MOG-IgG is of extrathecal origin. Serum MOG-IgG is present already at disease onset and remains detectable in the long-term course. Serum titers depend on disease activity and treatment status.

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Keywords {🔍}

mogigg, patients, samples, pubmed, article, myelitis, google, scholar, titers, serum, csf, antibodies, disease, study, neuromyelitis, optica, group, jarius, cas, aqpigg, control, positive, central, neurol, antibody, median, range, acute, clinical, cba, mogiggpositive, university, data, disorders, igg, attacks, andor, wildemann, part, onset, treatment, aquaporin, followup, mog, patient, neurology, nmo, negative, multiple, sclerosis,

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}^{\mathsf{2}}+\mathsf{6}\times \mathsf{1}{\mathsf{0}}^{{\textstyle \hbox{-}}\mathsf{6}}}-\mathsf{1} anti-n-methyl-d-aspartate receptor encephalitis n-methyl-d-aspartate receptor-igg [61] qmog-igg = csf/serum mog-igg ratio m1-aqp4-dna-transfected cells mog-igg-specific antibody index independent cell-based assays called cell-based assays qalb = csf/serum albumin ratio enzyme-linked immunosorbent assays mog-specific antibody index nmo-igg/aqp4-ab belongs complement-activating anti-mog antibodies live cell-based assay human full-length mog full-length human mog mock-transfected hek293 cells }}_{\mathsf{lim}\left appendix sections csf-restricted oligoclonal bands state privacy rights abbreviations adem mock-transfected control cells antibody index assessment detecting conformation-sensitive antibodies full size image myelin-oligodendrocyte glycoprotein antibodies drug-specific latency periods cd20-targeted immune therapy blood-csf barrier dysfunction mog-igg-positive isolated myelitis complement-activating igg1 subclass blood-csf barrier function lena-alexandra beume total-igg oligoclonal bands called ‘double-positive’ samples long-lived plasma cells mirjam korporal-kuhnke conclusion era-net e-rare 2 methodologically independent cba hek293 cells transfected anti-aquaporin-4 antibody production csf mog-igg belonged csf mog-igg belong mog-igg-seropositive patients 15 mog-igg-seropositive patients neuromyelitis optica mog-igg persisting mog-igg antibodies mog-igg serum titers

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         description:Antibodies to myelin oligodendrocyte glycoprotein (MOG-IgG) have been suggested to play a role in a subset of patients with neuromyelitis optica and related disorders. To assess (i) the frequency of MOG-IgG in a large and predominantly Caucasian cohort of patients with optic neuritis (ON) and/or myelitis; (ii) the frequency of MOG-IgG among AQP4-IgG-positive patients and vice versa; (iii) the origin and frequency of MOG-IgG in the cerebrospinal fluid (CSF); (iv) the presence of MOG-IgG at disease onset; and (v) the influence of disease activity and treatment status on MOG-IgG titers. 614 serum samples from patients with ON and/or myelitis and from controls, including 92 follow-up samples from 55 subjects, and 18 CSF samples were tested for MOG-IgG using a live cell-based assay (CBA) employing full-length human MOG-transfected HEK293A cells. MOG-IgG was detected in 95 sera from 50 patients with ON and/or myelitis, including 22/54 (40.7%) patients with a history of both ON and myelitis, 22/103 (21.4%) with a history of ON but no myelitis and 6/45 (13.3%) with a history of longitudinally extensive transverse myelitis but no ON, and in 1 control patient with encephalitis and a connective tissue disorder, all of whom were negative for AQP4-IgG. MOG-IgG was absent in 221 further controls, including 83 patients with AQP4-IgG-seropositive neuromyelitis optica spectrum disorders and 85 with multiple sclerosis (MS). MOG-IgG was found in 12/18 (67%) CSF samples from MOG-IgG-seropositive patients; the MOG-IgG-specific antibody index was negative in all cases, indicating a predominantly peripheral origin of CSF MOG-IgG. Serum and CSF MOG-IgG belonged to the complement-activating IgG1 subclass. MOG-IgG was present already at disease onset. The antibodies remained detectable in 40/45 (89%) follow-up samples obtained over a median period of 16.5 months (range 0–123). Serum titers were higher during attacks than during remission (p < 0.0001), highest during attacks of simultaneous myelitis and ON, lowest during acute isolated ON, and declined following treatment. To date, this is the largest cohort studied for IgG to human full-length MOG by means of an up-to-date CBA. MOG-IgG is present in a substantial subset of patients with ON and/or myelitis, but not in classical MS. Co-existence of MOG-IgG and AQP4-IgG is highly uncommon. CSF MOG-IgG is of extrathecal origin. Serum MOG-IgG is present already at disease onset and remains detectable in the long-term course. Serum titers depend on disease activity and treatment status.
         datePublished:2016-10-27T00:00:00Z
         dateModified:2016-10-27T00:00:00Z
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            Neuromyelitis optica (NMO)
            Devic’s syndrome
            Optic neuritis
            Transverse Myelitis
            Longitudinally extensive transverse myelitis (LETM)
            Neuromyelitis optica spectrum disorders (NMOSD)
            Multiple sclerosis
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            Neuromyelitis optica antibodies (NMO-IgG)
            Aquaporin-4 antibodies (AQP4-IgG)
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      headline:MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 1: Frequency, syndrome specificity, influence of disease activity, long-term course, association with AQP4-IgG, and origin
      description:Antibodies to myelin oligodendrocyte glycoprotein (MOG-IgG) have been suggested to play a role in a subset of patients with neuromyelitis optica and related disorders. To assess (i) the frequency of MOG-IgG in a large and predominantly Caucasian cohort of patients with optic neuritis (ON) and/or myelitis; (ii) the frequency of MOG-IgG among AQP4-IgG-positive patients and vice versa; (iii) the origin and frequency of MOG-IgG in the cerebrospinal fluid (CSF); (iv) the presence of MOG-IgG at disease onset; and (v) the influence of disease activity and treatment status on MOG-IgG titers. 614 serum samples from patients with ON and/or myelitis and from controls, including 92 follow-up samples from 55 subjects, and 18 CSF samples were tested for MOG-IgG using a live cell-based assay (CBA) employing full-length human MOG-transfected HEK293A cells. MOG-IgG was detected in 95 sera from 50 patients with ON and/or myelitis, including 22/54 (40.7%) patients with a history of both ON and myelitis, 22/103 (21.4%) with a history of ON but no myelitis and 6/45 (13.3%) with a history of longitudinally extensive transverse myelitis but no ON, and in 1 control patient with encephalitis and a connective tissue disorder, all of whom were negative for AQP4-IgG. MOG-IgG was absent in 221 further controls, including 83 patients with AQP4-IgG-seropositive neuromyelitis optica spectrum disorders and 85 with multiple sclerosis (MS). MOG-IgG was found in 12/18 (67%) CSF samples from MOG-IgG-seropositive patients; the MOG-IgG-specific antibody index was negative in all cases, indicating a predominantly peripheral origin of CSF MOG-IgG. Serum and CSF MOG-IgG belonged to the complement-activating IgG1 subclass. MOG-IgG was present already at disease onset. The antibodies remained detectable in 40/45 (89%) follow-up samples obtained over a median period of 16.5 months (range 0–123). Serum titers were higher during attacks than during remission (p < 0.0001), highest during attacks of simultaneous myelitis and ON, lowest during acute isolated ON, and declined following treatment. To date, this is the largest cohort studied for IgG to human full-length MOG by means of an up-to-date CBA. MOG-IgG is present in a substantial subset of patients with ON and/or myelitis, but not in classical MS. Co-existence of MOG-IgG and AQP4-IgG is highly uncommon. CSF MOG-IgG is of extrathecal origin. Serum MOG-IgG is present already at disease onset and remains detectable in the long-term course. Serum titers depend on disease activity and treatment status.
      datePublished:2016-10-27T00:00:00Z
      dateModified:2016-10-27T00:00:00Z
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      pageEnd:16
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12974-016-0717-1
      keywords:
         Neuromyelitis optica (NMO)
         Devic’s syndrome
         Optic neuritis
         Transverse Myelitis
         Longitudinally extensive transverse myelitis (LETM)
         Neuromyelitis optica spectrum disorders (NMOSD)
         Multiple sclerosis
         Autoantibodies
         Myelin oligodendrocyte glycoprotein antibodies (MOG-IgG)
         Neuromyelitis optica antibodies (NMO-IgG)
         Aquaporin-4 antibodies (AQP4-IgG)
         Cell-based assays
         Cerebrospinal fluid
         Antibody index
         Neurosciences
         Neurology
         Neurobiology
         Immunology
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