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.

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

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Figure Seropositivity for IgG against HSV-1, CMV, and EBV

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 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 3 Classical complement pathway activity and disease severity (A) Association between high innate classical pathway (CP) activity and degree of muscle.

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

Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.

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 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 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 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 Binding of the patient's IgG to Purkinje cells is inhibited by pretreatment of rat tissue with anti-VGCC antibodies, confirming specificity 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 Overview of the patient's history and immunofluorescence pattern of patient CSF IgG Overview of the patient's history and immunofluorescence pattern.

Figure 2 DTI values between the hepatitis C group and controls(A) DTI FA values, (B) DTI diffusion values. *Statistically significant at FDR-adjusted p.

Figure 1 Time points of blood sampling

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. Groups 1–3, patients tested, and test results (viral PCR and antibodies)‏ Groups 1–3, patients tested, and test results (viral PCR and antibodies)

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

Figure 1 Evolution of blood cell counts during 18-month treatment and follow-up (A) Mean white blood cell count, (B) mean lymphocyte count, (C) mean eosinophil.

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

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

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 1 Examination of MuSK antibody levels and B-cell subsetsFlow cytometric analysis (n = 13) using standardized Human Immunology Project Consortium.

Figure Overview of patients with demyelinating diseases, presence of clinical symptoms frequently associated with NMDAR encephalitis, and antibody status.

Figure 2 Longitudinal relationship between CSF glucose and protein changes Longitudinal relationship between CSF glucose and protein changes Delta glucose.

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 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 2 CD56bright natural killer (NK) cell counts in daclizumab high-yield process (DAC HYP)-treated patientsData are medians with 25th and 75th percentiles.

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

Figure Spinal cord imaging (A, B) Sagittal and axial T2-weighted cervical spine MRI demonstrating hyperintensities in the central gray matter of patient.

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 2 Kaplan-Meier survival curves for the fingolimod cohort In each graph, bottom tertile: solid line; middle tertile: long dashed line; top tertile:

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.

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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.

Gitanjali Das et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e453

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

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

Figure 2 Nonhuman primate brain immunohistochemistry

Figure 4 Venn diagram for B-cell Sup proteins compared with proteins from exosome-enriched fractions from a human B-cell line Venn diagram for B-cell Sup.

Figure 4 C5B3 decreased NMOSD mouse model lesions in vivo

N1 decoys differently inhibit ligand-induced NOTCH signaling.

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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 MOG detected with anti-human IgG (H + L) as the secondary antibody(A) Schematic of the human MOG proteins tested. The extracellular and transmembrane domains are identical, but the short-length MOG (SL-MOG) is 73 amino acids shorter at the C-terminus than full-length MOG (FL-MOG). (B) Screening 1,109 consecutive samples sent for aquaporin-4 (AQP4) antibody testing. With anti-human IgG (H + L) as the secondary antibody, 21 SL-MOG– positive samples and 180 FL-MOG–positive samples were identified; however, a cohort of epilepsy sera demonstrates the striking lack of specificity in the FL-MOG assay. Comparing the AQP4 seropositivity in the 2 MOG assays, 1/38 AQP4-positive samples were also positive for SL-MOG antibodies (C), compared with 10/38 for FL-MOG antibodies (D). CBA = cell-based assay. Patrick Waters et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e89 © 2015 American Academy of Neurology