Figure 1. Antibodies to MOG in a proportion of adult patients with MS

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Date of download: 6/30/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Quantification and Functional Characterization of.

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Copyright © 2010 American Medical Association. All rights reserved.

Figure EDSS, FS scores, and Modified MSFC scores

Figure 2. MRI features of patients with MS who had antibodies to myelin oligodendrocyte glycoprotein MRI features of patients with MS who had antibodies.

Figure 1. Absence of anti–neurofascin-155 (NF155) antibodies in combined central and peripheral demyelination (CCPD)‏ Absence of anti–neurofascin-155 (NF155)

Figure 2. Infliximab treatment effect

Figure 3 Brain MRI findings in patients with MOG-Ab Extensive brain lesions with large diameter (A and B), posterior reversible encephalopathy–like lesions.

Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.

Figure 3 B-cell amount and the frequency of various B-cell subtypes are differentially affected by FTY or DMF treatment B-cell amount and the frequency.

Figure 3 Antibodies to MOG using different secondary antibodies: Anti-human IgG (H + L), IgG1, or IgM(A) Comparison of binding to full-length myelin oligodendrocyte.

Figure 1 Percent positivity by clinical feature Overall, 6

Figure 3 Classical complement pathway activity and disease severity (A) Association between high innate classical pathway (CP) activity and degree of muscle.

Figure 2 Temporal distribution of MOG antibody in serum of 2 relapsing patients with demyelinating diseases Temporal distribution of MOG antibody in serum.

Figure Clinical course of acute neuritis and NMDA receptor (NMDAR) encephalitis, sural nerve biopsy, and detection of NMDAR antibodies(A) Approximately.

Figure 2 Expression of GABAA receptor and LGI1 by patient's thymomaTissue sections of the patient's thymoma incubated with biotinylated immunoglobulin.

Figure 2 NMDAR-Ab levels, clinical syndromes, and therapy in 8 informative patients with white matter syndromes in association with NMDAR-Ab NMDAR-Ab levels,

Figure 1 Flow diagram of the assays and the samples that were evaluatedA total of 1,109 samples were initially screened at a serum dilution of 1:20 for.

Figure 2 The frequency of helper T cells (Th) within CD4+ population and TCRγδ within CD3+ cells is affected by FTY and DMF treatment The frequency of.

Figure 2 Primary and secondary outcomes reported in multiple sclerosis (MS) disease-modifying therapy (DMT) clinical trials Primary and secondary outcomes.

Figure 1 Outcomes of greatest importance to selection of a multiple sclerosis (MS) disease-modifying therapy (DMT), as defined by persons with MS and panelists.

Figure 4 Abundance of cytokines which showed significant difference in expression in the plasma and the cultured PBMC of patients with RRMS Abundance of.

Figure 1 The abundance of CD3+ T cells and their subtypes are significantly affected by FTY and DMF treatment The abundance of CD3+ T cells and their subtypes.

Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer

Figure 1 8-Iso-PGF2α levels in CSF of patients with MS and controlsCSF 8-iso-prostaglandin F2α (8-iso-PGF2α) levels were estimated using an ELISA. (A)

Figure 2 Binding of the patient's IgG to Purkinje cells is inhibited by pretreatment of rat tissue with anti-VGCC antibodies, confirming specificity of.

Figure 2 Forest plots for subgroup analyses

Figure 2 Overview of the patient's history and immunofluorescence pattern of patient CSF IgG Overview of the patient's history and immunofluorescence pattern.

Figure 1 Characteristics of the German National MS Cohort

Figure 2 Concordance of results for commercial cell-based assay (CBA) and fluorescence-activated cell sorting (FACS) assays, FACS titers, and disease activity.

Figure 2 JCV index JCV index (A) Fifty samples of natalizumab-treated patients with multiple sclerosis were assessed twice for their anti-JCV antibody.

Figure 3 Cladogram indicating the effect of disease-modifying therapies on the phylogenetic structure of MS patients' microbiota Cladogram indicating the.

Figure 4 Pattern of relapse in patients with MOG-Ab Five myelin oligodendrocyte glycoprotein antibody (MOG-Ab)–positive patients experienced a relapse,

Figure 4 Aquaporin-4 immunoglobulin G (AQP4-IgG) index in time-matched paired serum-CSF specimens: 3 attack/preattack pairs and 7 bridge/remission pairs.

Figure 5 Increased B cell-activating factor (BAFF) levels are shared between immunomodulatory treatments Increased B cell-activating factor (BAFF) levels.

Figure 1 JCV serostatus JCV serostatus (A) Serostatus of 1,921 natalizumab-treated patients with multiple sclerosis, with JCV− patients shown in black.

Figure 5 Pairwise correlations between selected patient-reported outcomes and performance tests in patients with MS (A) The number of pairwise correlations.

Figure 3 Longitudinal performance of 2 MS–cohabitant participant pairs on Ishihara color testing Both response speed and response accuracy are provided.

Figure 4 Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis.

Figure Clinical and radiologic course(A) The T2 contrast-enhanced sequence on day 3 shows an extensive central cord lesion extending from C2 to T7. Clinical.

Figure 1 Kaplan-Meier estimation of time to neuromyelitis optica (NMO) conversion and development of motor disability Kaplan-Meier estimation of time to.

Figure 1 Responder rates of patients at 4 weeks compared with prevaccinated levels Responder rates of patients at 4 weeks compared with prevaccinated levels.

Figure 1 Proportions of the major B-cell subsets in DMF-treated patients Proportions of the major B-cell subsets in DMF-treated patients B cells were collected.

Figure 4 Shared and unique immune changes induced by multiple sclerosis (MS) immunomodulatory treatments Shared and unique immune changes induced by multiple.

Figure 1 Distribution of MOG IgG antibody in pediatric demyelinating diseases Distribution of MOG IgG antibody in pediatric demyelinating diseases (A)

Figure 1 Annual trend in specimen type submitted as first sample for aquaporin-4 immunoglobulin G testing (serum only vs CSF only vs both) from 101,065.

Figure 3 Correlation of lipid indexes to MRI measures of disease severity in multiple sclerosis Correlation of lipid indexes to MRI measures of disease.

Figure 1 Examples illustrating gating strategy for fluorescence-activated cell sorting (FACS)‏ Examples illustrating gating strategy for fluorescence-activated.

Figure 3 Multiple sclerosis (MS) immunomodulatory treatments interferon-β (IFNB) and fingolimod (FTY720) result in global perturbation of the immune system.

Figure 1 Relapse and rituximab historyThe figure shows rituximab (RTX) treatment history as well as relapse history for 100 days prior to the first RTX.

Figure 1 Anti-Epstein-Barr virus nuclear antigen-1 IgG quartile antibody status differences in MRI measures Anti-Epstein-Barr virus nuclear antigen-1 IgG.

Figure 1 Patterns of study retention The proportion of individuals actively participating in the study is displayed over the course of the study. Patterns.

Figure 3 Pedigrees of 3 multiplex families with NLRP3 mutations and MS The patient numbers refer to the patients listed in table 1. Pedigrees of 3 multiplex.

Figure Overview of patients with demyelinating diseases, presence of clinical symptoms frequently associated with NMDAR encephalitis, and antibody status.

Figure 2 Summary of the utility of MOG-Abs and OCB testing in predicting pediatric disease course at onset compared to clinical follow-up at 1 yearFollowing.

Figure 2 Correlation between wGRS and age at onset The figure shows the correlation between weighted genetic risk score (wGRS) and age at onset in all.

Figure Forty-two months of follow-up of clinical symptoms in parallel with therapeutic interventions and antibody titers/B-cell count Forty-two months.

Figure 1. Heat map of antibody binding patterns to glycolipid targets in Guillain-Barré syndrome (GBS) cases and controls Heat map of antibody binding.

Figure 4. The N:M ratio is significantly increased in patients with ALS and correlates with disease progression The N:M ratio is significantly increased.

Figure 1 Full-length MOG cell-based assay using a serum dilution of 1:160 as a cutoff for positivity (red line in both plots)(A) Myelin olidgodendrocyte.

Figure Avidity of IgG specific for influenza A and B following flu vaccinationAvidity of immunoglobulin (Ig) G specific for influenza A and B before and.

Figure 3 Effect of IVIg on endogenous relative concentration (in mAb equivalents) of JCV AbSix patients shown in this figure have had John Cunningham virus.

Figure Clinical course and overview of the treatment protocols♦ = neuroradiologic evidence of new disease activity; ★ = CD19+ reconstitution. Clinical.

Figure 3 DMF promotes an anti-inflammatory cytokine B-cell profile

Figure 2 Assessment of fluctuation in fatigue scores using environmental data The relationship between fatigue (as measured by the Modified Fatigue Impact.

Figure 2 Overview of apheresis therapies

Figure 6 Multiple target epitopes exist in the N-terminal domains of Caspr2 (A) Multidomain deletion constructs of Caspr2 were generated to determine which.

Figure 2 Cell-based assay demonstrating differential binding of AChR antibodies to the adult and fetal receptorsThe fetal (gamma subunit specific) and.

Figure 1 Cell gating and binding curve from FACS experiments and M23 and M1 antibody titers during relapses and remission Cell gating for fluorescence-activated.

Figure 1 Numbers/seropositivity rates of IVIg-naive and IVIg-exposed STRATIFY-2 enrollees* = % of enrollment samples, ** = date of IVIg and/or concentration.

Figure 2 Nonhuman primate brain immunohistochemistry

Presentation transcript:

Figure 1. Antibodies to MOG in a proportion of adult patients with MS Antibodies to MOG in a proportion of adult patients with MS (A) Sera from 3 groups of patients with MS were analyzed for anti-MOG reactivity. Group 1: patients with MS with a specific clinical phenotype, namely, with severe or recurrent myelitis and/or severe (visual acuity <0.5) or recurrent optic neuritis, and/or brainstem syndrome (n = 104). Group 2: unselected patients with MS matched for age and sex (n = 55). Group 3: biopsied patients (n = 22), 4 with MS type II pathology (empty triangles). The red line indicates the cutoff for anti-MOG positivity. Values shown for each anti-MOG IgG–positive patient represent the mean of 3 independent measurements using the first serum sample analyzed, which was 14, 16, 3, 18, and 9 years after disease onset for patients 1 through 5. (B, C) Clinical features, therapies, and longitudinal analysis of antibodies to MOG in patients 1 and 2. (D) Analysis of the epitope specificity of the MOG reactivity of the samples indicated with asterisks (*) in C. Reactivity of the serum samples diluted 1:50 to the indicated variants of hMOG and to mMOG is shown. Values obtained with wild-type hMOG were set as 100% and the other reactivities were calculated as described.22 Depicted are the mean values of 3 independent experiments ± SEM. DMF = dimethyl fumarate; DMT = disease-modifying therapy; EDSS = Expanded Disability Status Scale; FTY = fingolimod; GLAT = glatiramer acetate; hMOG = human myelin oligodendrocyte glycoprotein; IgG = immunoglobulin G; IVIG = IV immunoglobulins; MFI = mean fluorescence intensity; mMOG = mouse myelin oligodendrocyte glycoprotein; MOG = myelin oligodendrocyte glycoprotein; MS = multiple sclerosis; NAT = natalizumab; PLEX = plasma exchange; RX = rituximab. Melania Spadaro et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e257 © 2016 American Academy of Neurology