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

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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.

Antibodies to the GluN1 subunit of the N-methyl-d-aspartate (NMDA) receptor in a patient with anti-NMDA receptor encephalitis and ovarian teratoma. (A)

Okadaic-Acid-Induced Inhibition of Protein Phosphatase 2A Produces Activation of Mitogen-Activated Protein Kinases ERK1/2, MEK1/2, and p70 S6, Similar.

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

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

Figure. Patient imaging

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 2 Identification of synapsin Ia, Ib, and IIa as antigenic targets of IgA antibodies in CSF (A) Homogenates of mouse cerebellum and hippocampus as.

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 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 KCTD16 antibodies are associated with an underlying tumour

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 VGCC antibody uptake in cerebellar slice culture

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

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. 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 Reibergram (CSF/serum quotient diagram) of all included patients Increasing albumin quotients reflect increasing blood-brain barrier dysfunction.

Figure 1 Anti-LINGO-1 (Li81) has no effect on activated T-cell proliferation Anti-LINGO-1 (Li81) has no effect on activated T-cell proliferation (A) Western.

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 Clinical findings and CNS immunoreactivity of CSF IgA of a patient with limbic encephalitis (A) Cranial MRI of a 69-year-old man with limbic encephalitis.

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

Figure 1 Association between serum levels of IL-18 and hippocampal volume in patients with schizophrenia Scatter plots show a positive correlation between.

Figure Varicella-zoster virus antigen in the temporal artery, aorta, and carotid artery of a patient with refractory giant cell arteritis Immunohistochemical.

Figure 4 Autopsy immunochemistry results

Figure Disease course and neuropathology of CASPR2 encephalitis(A) Summary of the most important changes during the disease course. Disease course and.

Figure 3 ADAM22 mutant proteins do not bind to LGI1

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 Longitudinal relationship between CSF glucose and protein changes Longitudinal relationship between CSF glucose and protein changes Delta glucose.

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. Spinal cord MRI and immunofluorescence staining of the patient's serum and controls on different tissues and recombinant cell substrates Spinal.

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.

by Fei Chen, Paul W. Tillberg, and Edward S. Boyden

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

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

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 Clinical course and CSF/serum NMDA receptor (NMDAR) antibody (ab) titers of mother and infant Titers were measured with immunohistochemistry of.

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

Detection and classification of dendritic spines in transfected hippocampal neurons. Detection and classification of dendritic spines in transfected hippocampal.

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.

The Role of Selective Transport in Neuronal Protein Sorting

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.

EGF induces HPSE nucleolar localization in human BMBC cells.

BDNF protein is expressed in neurons and astrocytes of hippocampus after pilocarpine-induced SE. A, Representative confocal images of hippocampal subfields.

Figure Myelin binding of high-level MBP IgA antibodies from a patient with MS Myelin binding of high-level MBP IgA antibodies from a patient with MS (A)

Activation and expression of the transgene.

Presentation transcript:

Figure 3 Detection of synapsin Ia, Ib, and IIa in cell-based assays, colocalization of patient IgA and commercial synapsin antibodies in hippocampus sections and primary hippocampal neurons, and calculation of antibody indices (A) Human embryonal kidney (HEK293) cells transfected with synapsin (Syn) Ia, Ib, IIa, or IIb were fixed, permeabilized, and incubated with patient or control (CTL) CSF. Bound immunoglobulin A (IgA) was detected using an Alexa 594-coupled antihuman IgA secondary antibody. Detection of synapsin Ia, Ib, and IIa in cell-based assays, colocalization of patient IgA and commercial synapsin antibodies in hippocampus sections and primary hippocampal neurons, and calculation of antibody indices (A) Human embryonal kidney (HEK293) cells transfected with synapsin (Syn) Ia, Ib, IIa, or IIb were fixed, permeabilized, and incubated with patient or control (CTL) CSF. Bound immunoglobulin A (IgA) was detected using an Alexa 594-coupled antihuman IgA secondary antibody. An anti–green fluorescent protein (green fluorescent protein) antibody was used to enhance endogenous fluorescence of transfected cells. CSF IgA-stained cells expressing Syn Ia, Ib, and IIa, but not IIb. Cells incubated with control CSF showed no staining. (B) Left: Murine hippocampus sections were fixed, permeabilized, and incubated with patient CSF (dilution 1:100) and double-stained with a commercial antibody to both Syn I and Syn II, demonstrating colocalization of patient IgA and Syn I/II antibodies at the mossy fiber terminals in the stratum lucidum (Slu) of the CA3 region (boxed regions are depicted at higher magnification). Right: Staining of primary fixed and permeabilized murine hippocampal neurons with patient CSF and antibodies to microtubule-associated protein 2, a somatodendritic marker, showed a punctuate staining of CSF IgA along dendrites, indicative of a synaptic distribution. Double-staining of hippocampal neurons with patient CSF IgA and antibodies to Syn I/II revealed a complete overlap of signals. (C) IgA and immunoglobulin G (IgG) antibodies to Syn Ia/Ib in CSF and serum were titrated using cell-based assays and antibody indices were calculated as described in the Methods. The red line indicates the cutoff of 4, AI values above which indicate an intrathecal antibody synthesis. There was a strong intrathecal synthesis of IgA and IgG to Syn Ia/Ib throughout the course of the disease. CA = cornu ammonis; Map2 = microtubule-associated protein 2. Johannes Piepgras et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e169 © 2015 American Academy of Neurology