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.

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

Figure Model contrasting the potential role of antibodies to myelin oligodendrocyte glycoprotein (MOG) or aquaporin-4 (AQP4) in opticospinal inflammationMOG-specific.

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 1 Stiff-person syndrome spectrum patient serum bound to membranes of live GlyRα1-transfected HEK293 cells Stiff-person syndrome spectrum patient.

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

Figure 2 Serums of patients with stiff-person syndrome spectrum disorders containing GlyRα1-Binding IgG specifically induces internalization of GlyRα1.

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 5 Treatment with fingolimod raises the activation threshold of monocytes in MS Peripheral blood mononuclear cells from 8 healthy donors, 7 patients.

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

Figure 3 Decreased AHI1 in human CD4+ T cells is associated with decreased proliferation and increased IFNγ production Decreased AHI1 in human CD4+ T cells.

Figure DPPX antibodies as detected by fluorescence-based immunohistochemistry and a cell-based assayImmunohistochemistry displayed binding of the patient's.

Figure 2 M1 and M23 AQP4 isoforms compared by freeze-fracture electron microscopic and Western blot analyses M1 and M23 AQP4 isoforms compared by freeze-fracture.

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 Neuromyelitis optica spectrum disorder (NMOSD) subgroups and patients with relapsing-remitting multiple sclerosis (RRMS) show different antibody.

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 2 Elevated antibody reactivities against myelin and Epstein-Barr virus (EBV) peptides in relapsing-remitting multiple sclerosis (RRMS) and higher.

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 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 3 Effects of RTX on specific anti-pathogen IgGs

Figure 2. ROC curves for different group comparisons

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 GABAB expression in the thymus(A–C) Staining of thymus tissue with anti-cytokeratin (A) and anti-GABAB antibody (B, C double immunofluorescence).

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

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 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 3 Detection of synapsin Ia, Ib, and IIa in cell-based assays, colocalization of patient IgA and commercial synapsin antibodies in hippocampus sections.

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. 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 4 Purified IgG from DEM patients induces loss of cytoskeleton organization in live human oligodendroglial MO3.13MOG+ cells Purified IgG from DEM.

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

Figure 2 P2Y12 expression is upregulated in M2-polarized human microglia(A, B) Using TaqMan quantitative real-time PCR, P2Y12 expression was measured in.

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 2 Comparison of BAFF levels in controls and patients with MuSK(A) ELISA performed on plasma samples shows higher B cell–activating factor (BAFF)

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 1 Determination of anti-Tr/DNER by indirect immunofluorescence(A) Slide with 10 reaction fields as used for the study. Determination of anti-Tr/DNER.

Figure 2. Detection of KIR4.1 autoantibodies using LIPS

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 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 Natalizumab increases expression of proinflammatory genes and cytokines by CD49d+ memory CD4 cells Natalizumab increases expression of proinflammatory.

Figure 2 C5B3 prevented AQP4-IgG–mediated CDC without affecting AQP4-IgG binding to AQP4 C5B3 prevented AQP4-IgG–mediated CDC without affecting AQP4-IgG.

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

Figure 3 Fluorescence-activated cell sorting (FACS) employing cells singly transfected with M1-AQP4 or M23-AQP4 or cotransfected with both AQP4 isoforms.

Figure 1. MBP-specific IFN-γ+ but not IL-17+ frequencies are significantly different between patients with MS and HCs MBP-specific IFN-γ+ but not IL-17+

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

Figure 2 B-cell very late antigen-4 (VLA-4) deficiency reduced CNS accumulation of B cells, but not proinflammatory or regulatory T cells (Treg), in myelin.

Figure 2 Detection of atypical anti-neuronal antibodies Immunohistofluorescence assay on rat brain sagittal slices incubated with the patient's CSF and.

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 3. Sensitivity and specificity of microarray analysis in relation to target number Sensitivity and specificity of microarray analysis in relation.

Figure 3 Alemtuzumab-induced changes in monocytes

Figure 3 C5B3 blocked MAC formation

Figure 2 Antibodies to MOG detected with anti-human IgG (H + L) as the secondary antibody(A) Schematic of the human MOG proteins tested. Antibodies to.

Figure 2 Nonhuman primate brain immunohistochemistry

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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 glycoprotein (FL-MOG) using anti-human IgG (H + L), anti-IgM, or anti-IgG1 secondary antibodies with 3 different test sera (a-c) and a healthy control serum (con). Antibodies to MOG using different secondary antibodies: Anti-human IgG (H + L), IgG1, or IgM(A) Comparison of binding to full-length myelin oligodendrocyte glycoprotein (FL-MOG) using anti-human IgG (H + L), anti-IgM, or anti-IgG1 secondary antibodies with 3 different test sera (a-c) and a healthy control serum (con). (B) IgM and (C) IgG1 binding scores for patients and healthy controls (HC). (D.a) PIRES2-DsRed2-FL-MOG transiently transfected HEK cells are separated into cells that express MOG and DsRed2 well (in the upper section of the graph) or poorly or not at all (lowest section of the graph). (D.b) Healthy control sera (upper panels) causes a specific shift in the MOG-transfected cells compared to the untransfected cells when anti-human IgG (H + L) or anti-human IgM secondary antibodies are used (arrows), but not when anti-human IgG1 secondary antibodies are used. The lower panels show higher shifts in sera positive for FL-MOG antibodies compared to controls in the upper panel. (E) Fifteen samples that were IgG (H + L) positive and 5 healthy controls were tested on flow cytometry with anti-IgM or IgG1. A high cutoff is generated with anti-human IgM secondary antibody (ΔMFI of 270) vs a ΔMFI of 2.5 for the anti-human IgG1 antibody. Of note, one IgM-positive patient is IgG1 negative (blue circle). Ab = antibody; AQP4 = aquaporin-4; CBA = cell-based assay; MFI = mean fluorescence intensity; MS = multiple sclerosis. Patrick Waters et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e89 © 2015 American Academy of Neurology