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.

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Figure 2 ERG amplitude reduction in the follow-up study

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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)

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 1 Muscle biopsy from a patient with a slowly progressive (24 years) HMGCR antibody–associated myopathy syndrome (A) Hematoxylin & eosin stain, (B)

Figure 2 GlyR antibody binding

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. Change in total PSPRS score from baseline to each study visit for all participants Change in total PSPRS score from baseline to each study visit.

Figure 3 Immunohistochemical analyses of positive and negative Epstein-Barr virus (EBV) control tissues using immunostaining Immunohistochemical analyses.

Figure 1 Percent positivity by clinical feature Overall, 6

Figure 1 Treg percentage and suppressive function increased during each round of Treg infusions Treg percentage and suppressive function increased during.

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 Immunopathologic analysis of all 3 Rasmussen encephalitis cases Immunopathologic analysis of all 3 Rasmussen encephalitis cases (A) Perivascular.

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 4 Detection of EBER+ cells in MS and control brains by in situ hybridization Detection of EBER+ cells in MS and control brains by in situ hybridization.

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 Brain MRI and biopsy specimens from the pontine lesion

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

Figure Nuclear Nrf2 expression after fumarate therapy A new left occipital fluid-attenuated inversion recovery hyperintense (A), T1 hypointense (B), and.

Figure 2 Neuropathologic examination for lymphoma etiology (patients 1–4)‏ Neuropathologic examination for lymphoma etiology (patients 1–4) Immunohistochemical.

Figure 4 Comparison of 7.0T and 3.0T MRI (patients 5 and 6)‏

Figure 2 Neuropathology of PML lesions in a patient with MS treated with fingolimod Neuropathology of PML lesions in a patient with MS treated with fingolimod.

Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer

Figure 2 Histochemical and immunohistochemical staining and electron microscopic examination of structures in the brain biopsy Hematoxylin & eosin staining.

Figure 4 Neuropathology of MOG and AQP4 antibody–associated demyelinating lesions in the brain The biopsy specimen revealed a small actively demyelinating.

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 MRI and neuropathologic characteristics of the tumefactive demyelinating lesion in our patient MRI and neuropathologic characteristics of the tumefactive.

Figure MRI and histology of demyelinating lesion(A) Symmetric T2 hyperintensity in the midbrain with relative sparing of cerebral peduncles. MRI and histology.

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 4 Representative images of skin biopsy sample

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 3. Time curves for GFAP, S100B, and tTau release in CSF

Figure 3 Detection of JC virus (JCV) genomic DNA in mildly enlarged nuclei of oligodendroglia-like cells Detection of JC virus (JCV) genomic DNA in mildly.

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 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 2 Abnormal myofiber nuclei in HMGCR antibody–associated myopathy Myonuclei are often enlarged (dark arrow) with clear centers (dark arrowhead) or.

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 Kaplan-Meier estimation of time to neuromyelitis optica (NMO) conversion and development of motor disability Kaplan-Meier estimation of time to.

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. Radiologic and pathologic findings

Figure 4 Autopsy immunochemistry results

Figure Leptomeningeal inflammationPostcontrast T1-weighted MRI: abnormal leptomeningeal enhancement over the frontoparietal lobes and interhemispheric.

Figure 2 Induced deletion of CXCR2 on oligodendrocyte lineage cells after tamoxifen injection in Cxcr2-cKO mice Induced deletion of CXCR2 on oligodendrocyte.

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 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 MRI brain comparison prior and after treatment and brain biopsy findings MRI brain comparison prior and after treatment and brain biopsy findings.

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 Brain biopsy of 2 patients with anti-MOG encephalitis initially misdiagnosed with small vessel CNS vasculitis Brain biopsy of 2 patients with.

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 Muscle biopsy showing myofiber atrophy and degeneration

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.

Yian Gu et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e521

Ingo Kleiter et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e504

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 6 P2Y12 is highly expressed in CD68+ and CD163+ cells during parasitic brain infectionIn a case of Schistosoma mekongi infection, hematoxylin and.

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

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

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

Immunoreactivity for the lipocalin 2 (LCN2) receptor (SLC22A17), glial fibrillary acidic protein (GFAP), Iba-1 and neuronal nuclei (NeuN) 24 h after intraventricular.

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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 AQP4 immunoreactivity with myelin pallor is shown (surrounded by arrows). (B) Staining with glial fibrillary acidic protein (GFAP) (brown) is shown. Loss of GFAP immunoreactivity is observed in the corresponding area shown in A (surrounded by arrows). Scale bar: 50 μm. Takuya Uehara et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e230 © 2016 American Academy of Neurology