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)

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Figure Seropositivity for IgG against HSV-1, CMV, and EBV
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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 4. Brain imaging and neuropathologic demonstration of Epstein-Barr virus (EBV) encephalitis in patient PT-10 Brain imaging and neuropathologic demonstration.
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 3 Immunohistochemical analyses of positive and negative Epstein-Barr virus (EBV) control tissues using immunostaining Immunohistochemical analyses.
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 4 Relation of neuropsychological deficits and intrathecal immune cell subsets in GABAB receptor antibody–associated limbic encephalitis Relation.
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 3 JCV index changes in JCV+ patients
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 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 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 Elevated antibody reactivities against myelin and Epstein-Barr virus (EBV) peptides in relapsing-remitting multiple sclerosis (RRMS) and higher.
Figure 5 Increased frequency of parenchymal CD138- and LMP-1–positive cells in MS Increased frequency of parenchymal CD138- and LMP-1–positive cells in.
Figure 1 MOR103 sequential-dose trial flowchart of study population with multiple sclerosis aPatients received 2 doses of study drug before trial withdrawal.
Figure 3 Gene expression in CSF cell pellets
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 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 2 JCV index JCV index (A) Fifty samples of natalizumab-treated patients with multiple sclerosis were assessed twice for their anti-JCV antibody.
Figure 2 CD4+ and CD8+ T cells accumulate in the CSF in GABAB receptor antibody–associated LE CD4+ and CD8+ T cells accumulate in the CSF in GABAB receptor.
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 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 4 Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis.
Figure Time course of the patient's diagnostics and treatment
Figure 2 Relative concentration (in mAb equivalents) of JCV Ab in samples tested prior to IVIg (“pre-IVIg”), within 30 days of IVIg (“during IVIg”), and.
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 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 B cells and plasma cells accumulate in the CSF in GABAB receptor antibody–associated LE B cells and plasma cells accumulate in the CSF in GABAB.
Figure 2 Immunohistological detection of EBV latent and early lytic proteins in MS and control brains Immunohistological detection of EBV latent and early.
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 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 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 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 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 1 Follow-up periods of 33 anti–3-hydroxy-3-methylglutaryl coenzyme A reductase autoantibody (HMGCR Ab+) myopathy patients in relation to cancer.
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.
Gitanjali Das et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e453
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 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 1 Numbers/seropositivity rates of IVIg-naive and IVIg-exposed STRATIFY-2 enrollees* = % of enrollment samples, ** = date of IVIg and/or concentration.
Figure (A and B) Effect of canakinumab in muscle strength measured in each patient as mean bilateral GF (A) and TMS (B) during the mean study period of.
Figure 1 Standard treatment scheme and antibody titer changes
Presentation transcript:

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) Ab = antibody; AMPA-R = amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor; ANA = antinuclear antibody; CBA = cell-based assay; CSFs = CSF specimens; EBV = Epstein-Barr virus; GABAB-R = γ-aminobutyric acid type B receptor; GPC = gastric parietal cell; HHV-6 = human herpes virus 6; HSV = herpes simplex virus; IFA = immunofluorescence assay; IgG = immunoglobulin G; NMDA-R = NMDA receptor; PCR = polymerase chain reaction; SMA = smooth muscle antibody; UNA = uncharacterized neural antibody. Jenny J. Linnoila et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e245 © 2016 American Academy of Neurology