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

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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)

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Nat. Rev. Neurol. doi: /nrneurol

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 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 2 Anti-LINGO-1 (Li81) does not affect cytokine production

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.

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

Figure 1 Histopathologic features of a chronic active and a chronic plaque in the MS brain Histopathologic features of a chronic active and a chronic plaque.

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 2 Brain-infiltrating immune cells mainly consist of CD8+ memory T cells Immunofluorescence staining of brain-infiltrating immune cells. Brain-infiltrating.

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 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 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 Mean serum concentrations of BIIB033 vs time(A) Single ascending dose study and (B) multiple ascending dose study. Mean serum concentrations of.

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

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

Figure 1 VGCC antibody uptake in cerebellar slice culture

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 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 1 Phenotype and functional properties of B cells in MS and HCs at baseline Phenotype and functional properties of B cells in MS and HCs at baseline.

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 2 Reduced frequency of central memory CD4 T cells in patients with PML Reduced frequency of central memory CD4 T cells (CD4Tcm) (p < ), naive.

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

Figure 2 Immunohistological detection of EBV latent and early lytic proteins in MS and control brains Immunohistological detection of EBV latent and early.

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 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 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 1 Clinical status and autoantibody titers in rituximab-treated patients with anti-CNTN1/NF155 chronic inflammatory demyelinating polyneuropathy.

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 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 2 Histopathological features in CIDP

Figure 1 Volcano plot Peptides (n = 2,260) showing distribution of fold change and statistical significance. Volcano plot Peptides (n = 2,260) showing.

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

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

Figure 3 Fingolimod inhibits TNF-α secretion by human monocytes Peripheral blood mononuclear cells from healthy donors were briefly exposed to increasing.

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 2 Detection of slanDCs in CSF of patients with MS(A, B) Immunocytochemical stainings were performed to determine the presence of 6-sulfo LacNAc+

Figure 3 C5B3 blocked MAC formation

Figure 2 Time from incident ADS event to MS diagnosis

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

Figure 3. Verification of GluRd2 as the target antigen of the patient's antineural autoantibodies Verification of GluRd2 as the target antigen of the patient's.

Figure 4 Longitudinal analysis of peripheral immune cell composition Frequency of naive, central memory (Tcm), and effector memory (Tem) CD4 T cells over.

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Figure 1. Absence of anti–neurofascin-155 (NF155) antibodies in combined central and peripheral demyelination (CCPD)‏ Absence of anti–neurofascin-155 (NF155) antibodies in combined central and peripheral demyelination (CCPD) (A) Clinical features of the patients with CCPD. EMRN = encephalomyeloradiculoneuritis; IVIG = IV immunoglobulin; MRN = myeloradiculoneuritis; PNS = peripheral nervous system. (B–E) Serum samples from patients with CCPD (n = 16), patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) (n = 26), patients with other peripheral neuropathy (PN) (n = 15), patients with multiple sclerosis (MS) (n = 15), and healthy controls (HC) (n = 20) were tested for autoantibodies to rat NF155 (B) and human NF155 (C) by ELISA. Optical densities (OD) to NF155 are shown after subtraction of baseline OD reading to bovine serum albumin. The cutoff (red line) represents the mean of HC and other PN groups plus 3 standard deviations. (D) Serum from NF155-positive patients with CIDP, but not sera of patients with CCPD, reacted against myc-tagged human NF155 in HEK293 cells. (E) NF155-positive CIDP serum, but not sera of patients with CCPD, colocalized with contactin-1, an axonal protein that interacts with glial NF155 at paranodes, in mouse sciatic nerve fibers. Scale bars (D, E): 10 μm. Andrea Cortese et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e238 © 2016 American Academy of Neurology