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

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

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Figure 2 ALSFRS-R changes (A) Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) slope after 6 months of treatment without (left)

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 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 Brain MRI of the patient throughout the disease course(A) Brain MRI at the time of cerebral toxoplasmosis diagnosis (a) and after 1 month of toxoplasmosis.

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

Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.

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

Figure 3 Multifocal visual-evoked potentials in optic neuritis Figure shows the visual-evoked potentials (VEPs) in 52 sectors of the retina. Multifocal.

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 Brain biopsy Brain biopsy (A) Double staining with anti-aquaporin-4 (AQP4) antibody (dark green) and Luxol fast blue (blue) is shown. Loss of.

Figure 1 Cerebral MRI during the disease course Cerebral MRI with multiple cerebral supratentorial lesions during the disease course: periventricular lesions.

Figure 1 Evolution of visual function after acute optic neuritis Figure shows the measurement of high-contrast visual acuity (VA) using the Early Treatment.

Figure 2 APCs from laquinimod-treated mice inhibit differentiation of Tfh cells APCs from laquinimod-treated mice inhibit differentiation of Tfh cells.

Figure 1 MOR103 sequential-dose trial flowchart of study population with multiple sclerosis aPatients received 2 doses of study drug before trial withdrawal.

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

Figure 3 EEG demonstrating ictal seizure discharges in a patient with faciobrachial dystonic seizures The EEG of a 56-year-old woman with faciobrachial.

Figure 1 Peripheral blood leukocyte subset counts during dimethyl fumarate treatmentComplete blood cell counts were obtained at baseline (n = 34) and at.

Figure 2 DTI values between the hepatitis C group and controls(A) DTI FA values, (B) DTI diffusion values. *Statistically significant at FDR-adjusted p.

Figure 1 Characteristics of the German National MS Cohort

Figure 1 Time points of blood sampling

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

Figure 1 White matter lesion central vein visibility in MS and absence in small vessel disease (SVD)‏ White matter lesion central vein visibility in MS.

Figure 1 Schematic overview of flow cytometry Schematic overview on the analysis of peripheral immune cells by flow cytometry. Schematic overview of flow.

Figure 1 Evolution of blood cell counts during 18-month treatment and follow-up (A) Mean white blood cell count, (B) mean lymphocyte count, (C) mean eosinophil.

Figure Family tree with the HLA haplotyping of 6 members of the family

Figure 2 Cerebral and spinal MRI (A) Restricted diffusion of both optic nerves (arrows) on diffusion-weighted and apparent diffusion coefficient imaging.

Figure 2. Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem.

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

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 1 Imaging of disease onset and treatment response Repeat MRI scans including fluid-attenuated inversion recovery (FLAIR) (A) and T2 fast field echo.

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 Examination of MuSK antibody levels and B-cell subsetsFlow cytometric analysis (n = 13) using standardized Human Immunology Project Consortium.

Figure 2 Clinical and autoantibody status of 2 CNTN1 or NF155+ patients not receiving rituximab Despite corticosteroids and methotrexate treatment, patient.

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 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 1 CD52 expression on innate myeloid and lymphoid cell subsets

Figure 2 Assessment of systemic disease activityTc99 scintigraphy (A) and fluorodeoxyglucose PET imaging (B, C) at disease onset 2 years before acute deterioration.

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 2 Repopulation of CD19+ cells in low and high BSA patients and calculation of the BSA Repopulation of CD19+ cells in low and high BSA patients and.

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 2 CD56bright natural killer (NK) cell counts in daclizumab high-yield process (DAC HYP)-treated patientsData are medians with 25th and 75th percentiles.

Figure 1 Peripheral blood lymphocyte counts during dose titrationB-lymphocyte (CD19+; A) and total lymphocyte (CD45+; B) counts (cells/µL) in peripheral.

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

Figure Spinal cord imaging (A, B) Sagittal and axial T2-weighted cervical spine MRI demonstrating hyperintensities in the central gray matter of patient.

Figure 2 Brain biopsy of 2 patients with anti-MOG encephalitis initially misdiagnosed with small vessel CNS vasculitis Brain biopsy of 2 patients with.

Figure 1 Classical pathway and lectin pathway activity in patients with multifocal motor neuropathy and controls Classical pathway (CP) activity (A) and.

Figure 2 Overview of apheresis therapies

Yian Gu et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e521

Ingo Kleiter et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e504

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

Gitanjali Das et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e453

Figure 3 Freedom from clinical disease activity during 36 months of fingolimod treatment Freedom from clinical disease activity during 36 months of fingolimod.

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

Figure 2. Percentage of CD16− monocytes in the blood is reduced during disease progression Percentage of CD16− monocytes in the blood is reduced during.

Figure (A and B) Effect of canakinumab in muscle strength measured in each patient as mean bilateral GF (A) and TMS (B) during the mean study period of.

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Figure 4 Pattern of relapse in patients with MOG-Ab Five myelin oligodendrocyte glycoprotein antibody (MOG-Ab)–positive patients experienced a relapse, all of which manifested as optic neuritis (ON). Pattern of relapse in patients with MOG-Ab Five myelin oligodendrocyte glycoprotein antibody (MOG-Ab)–positive patients experienced a relapse, all of which manifested as optic neuritis (ON). All patients with a relapsing disease course experienced a relapse within the first year of disease onset. Blue bar represents treatment period for relapse prevention. Sung-Min Kim et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e163 © 2015 American Academy of Neurology