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

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1 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

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

Date of download: 6/30/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Quantification and Functional Characterization of.
Copyright © 2010 American Medical Association. All rights reserved.

Copyright © 2010 American Medical Association. All rights reserved.
Figure EDSS, FS scores, and Modified MSFC scores

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

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