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

Published byRené Bauwens Modified over 5 years ago

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Presentation on theme: "Figure 1 Distribution of MOG IgG antibody in pediatric demyelinating diseases Distribution of MOG IgG antibody in pediatric demyelinating diseases (A)"— Presentation transcript:

1 Figure 1 Distribution of MOG IgG antibody in pediatric demyelinating diseases
Distribution of MOG IgG antibody in pediatric demyelinating diseases (A) Antibody reactivity to myelin oligodendrocyte glycoprotein (MOG) was determined by flow cytometry live cell-based assay. (B) Representative example of flow cytometry histograms for one MOG antibody–positive patient with a very high ΔMFI and (C) an intermediate ΔMFI. MFI values are noted in the legend. (D) Human surface MOG IgG antibody was detected in 31/73 sera from patients with demyelinating diseases (DEM) and 0/24 controls (CTL). Magenta line on graph represents the positivity threshold. MOG antibody positivity is shown between brackets. (E) Surface MOG antibody was detected in 3/22 CSF from patients with DEM and 0/20 CSF from patients with other neurologic diseases (CTL). Black circles represent patients with positive MOG antibody in CSF and in serum. (F) Distribution and number of MOG antibody–positive patients in optic neuritis (ON). (G) Correlation between erythrocyte sedimentation rate and age in MOG antibody–positive patients. (H) Distribution and (I) number of MOG antibody–positive patients in demyelinating diseases at follow-up. Ab = antibody; ADEM = acute disseminated encephalomyelitis; CIS = clinically isolated syndrome; BON = bilateral optic neuritis; HEK = human embryonic kidney; Ig = immunoglobulin; MFI = mean fluorescence intensity; MS = multiple sclerosis; TM = transverse myelitis; UON = unilateral optic neuritis. Russell C. Dale et al. Neurol Neuroimmunol Neuroinflamm 2014;1:e12 © 2014 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 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 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 GlyR antibody binding

Figure 2 GlyR antibody binding
Figure 1 Stiff-person syndrome spectrum patient serum bound to membranes of live GlyRα1-transfected HEK293 cells Stiff-person syndrome spectrum patient.

Figure 1 Stiff-person syndrome spectrum patient serum bound to membranes of live GlyRα1-transfected HEK293 cells Stiff-person syndrome spectrum patient.
Figure 2 Association of serum IgG reactivity with MRI measures of disease severity Association of serum IgG reactivity with MRI measures of disease severity.

Figure 2 Association of serum IgG reactivity with MRI measures of disease severity Association of serum IgG reactivity with MRI measures of disease severity.
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 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 2 Serums of patients with stiff-person syndrome spectrum disorders containing GlyRα1-Binding IgG specifically induces internalization of GlyRα1.

Figure 2 Serums of patients with stiff-person syndrome spectrum disorders containing GlyRα1-Binding IgG specifically induces internalization of GlyRα1.
Figure 3 Archetypal MS clinical course depicted over 20 years

Figure 3 Archetypal MS clinical course depicted over 20 years
Figure 1 Percent positivity by clinical feature Overall, 6

Figure 1 Percent positivity by clinical feature Overall, 6
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 DPPX antibodies as detected by fluorescence-based immunohistochemistry and a cell-based assayImmunohistochemistry displayed binding of the patient's.

Figure DPPX antibodies as detected by fluorescence-based immunohistochemistry and a cell-based assayImmunohistochemistry displayed binding of the patient's.
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 Reactivity of the patients' antibodies with rat brain and HEK cell-based assays Rat hippocampal dentate gyrus neuropils were stained with patient.

Figure 1 Reactivity of the patients' antibodies with rat brain and HEK cell-based assays Rat hippocampal dentate gyrus neuropils were stained with patient.
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 APCs from laquinimod-treated mice inhibit differentiation of Tfh cells APCs from laquinimod-treated mice inhibit differentiation of Tfh cells.

Figure 2 APCs from laquinimod-treated mice inhibit differentiation of Tfh cells APCs from laquinimod-treated mice inhibit differentiation of Tfh cells.
Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer

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

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