Figure 1 Integrative model of NMO/SD pathogenesis

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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 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.

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 1 Percent positivity by clinical feature Overall, 6

Figure Brain MRI of the patient throughout the disease course(A) Brain MRI at the time of cerebral toxoplasmosis diagnosis (a) and after 1 month of toxoplasmosis.

Figure 2 Comparative milestones in T and B lymphocyte maturation

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Figure 1 Neuromyelitis optica spectrum disorder (NMOSD) subgroups and patients with relapsing-remitting multiple sclerosis (RRMS) show different antibody.

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 Correlation between total IgG levels and anti-AQP4 IgG titer

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Figure 4 Pattern of relapse in patients with MOG-Ab Five myelin oligodendrocyte glycoprotein antibody (MOG-Ab)–positive patients experienced a relapse,

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Figure 2 Cerebral and spinal MRI (A) Restricted diffusion of both optic nerves (arrows) on diffusion-weighted and apparent diffusion coefficient imaging.

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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.

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Figure 4 Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis.

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Figure 7 VEGF as a mediator of neuroinflammatory disease

Figure 2 Immune changes in peripheral blood of pregnant patients with NMO Immune changes in peripheral blood of pregnant patients with NMO (A) Interleukin.

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.

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Figure 2 CD4+ T-cell subsets fluorescence-activated cell sorting analysis in peripheral blood mononuclear cells of patients with multiple sclerosis treated.

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Figure 1 Annualized percentage brain volume change

Figure 2 Evolution of blood cell counts during interleukin (IL)–7 therapy Evolution of blood cell counts during interleukin (IL)–7 therapy The leukocyte.

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

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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.

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Figure 2 Detection of atypical anti-neuronal antibodies Immunohistofluorescence assay on rat brain sagittal slices incubated with the patient's CSF and.

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

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Figure 3 Alemtuzumab-induced changes in monocytes

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 4 Cell count of selective immune cell subpopulations during alemtuzumab Cell count of selective immune cell subpopulations during alemtuzumab Absolute.

Figure 5 C5B3 inhibited inflammatory infiltration in an NMOSD mouse model in vivo C5B3 inhibited inflammatory infiltration in an NMOSD mouse model in vivo.

Figure 2 Time from incident ADS event to MS diagnosis

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

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

Presentation transcript:

Figure 1 Integrative model of NMO/SD pathogenesis Integrative model of NMO/SD pathogenesis Distinct stages of disease are illustrated as relative temporal and spatial comparators in NMO/SD progression. Note that over the course of disease progression and demyelination, additional autoantigens may be revealed and/or recognized, potentially resulting in antigen spreading and expansion/compounding of autoreactivity. A = astrocyte (AQP4-expressing cells that support neuronal viability and function); AQP4 = aquaporin 4; B = B lymphocyte; BBB = blood-brain barrier; E = eosinophil; M = monocyte/macrophage; N = neuron; NK = natural killer cell; NMO/SD = neuromyelitis optica/spectrum disorder; P = polymorphonuclear leukocyte (neutrophil); PER = periphery; T = T lymphocyte. Larry Steinman et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e276 © 2016 American Academy of Neurology