Figure 2 Nonhuman primate brain immunohistochemistry

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Figure 2 ERG amplitude reduction in the follow-up study

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 Medial occipital lobe (designated by visual cortical brain regions) hypometabolism in anti–NMDA receptor encephalitis Medial occipital lobe (designated.

Figure 1 Box plot of the venous diameter in lesions

Figure 1 Regional changes in FA values

Figure 1 Immunofluorescence pattern of patient septin-5-immunoglobulin G binding to mouse tissues Immunofluorescence pattern of patient septin-5-immunoglobulin.

Figure 1 Stiff-person syndrome spectrum patient serum bound to membranes of live GlyRα1-transfected HEK293 cells Stiff-person syndrome spectrum patient.

Figure MRI of anti-MOG-IgG–associated myelitis

Figure 2 Spinal cord lesions

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

Figure 4 Correlation of age with [11C](R)-PK11195 binding in the normal-appearing white matter (NAWM) and thalami Correlation of age with [11C](R)-PK11195.

Figure 1 Coronal MRI images showing the evolution of white matter abnormality and atrophy of patient 1 Coronal MRI images showing the evolution of white.

Figure 2 Disease progression slowed during each round of Treg infusions and correlated with increased Treg suppressive function Disease progression slowed.

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

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

Figure 1 Comparison of miR-150-5p (log scale), prednisone dose (mg), and QMG score between the thymectomy (ETTX) and prednisone groups Comparison of miR-150-5p.

Figure 2 Neurochemical profiles for each neurocognitive trajectory

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 ERG peak time delay at baseline

Figure 1 Linear relationship between CSF inflammation and glucose in meningitis; analysis stratified by diagnostic category (aseptic, n = 115 and microbial,

Figure 3 Gene expression in CSF cell pellets

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

Figure Association of hippocampal subfield volumes to cognition by neopterin level, volumes, and cognition adjusted for age, education, race, sex, and.

Figure 3 Effects of RTX on specific anti-pathogen IgGs

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Figure 3 Temporal trends in FALS incidence

Figure 1 White matter lesion central vein visibility in MS and absence in small vessel disease (SVD)‏ White matter lesion central vein visibility in MS.

Figure 3 sVEGF concentrations in anemia and hypoxemic diseases

Figure 1 Radiologic features of human myelin oligodendrocyte glycoprotein immunoglobulin G–positive patients with cranial nerve involvement Radiologic.

Figure Family tree with the HLA haplotyping of 6 members of the family

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

Figure 4 Voltage-clamp recordings of KCNJ18 carrying the patient's SNVs expressed in Xenopus laevis oocytes under control conditions and after application.

Figure 1 Patients with acute anti–NMDA receptor encephalitis have marked hypometabolism of the visual cortical brain region correlating with the medial.

Figure Alluvial plot of modified Rankin Scale (mRS) scores during and at the end of hospital stay Alluvial plot of modified Rankin Scale (mRS) scores during.

Figure 4 Leukocyte subset isolation from brain tissue by enzymatic dissociation Leukocyte subset isolation from brain tissue by enzymatic dissociation.

Figure 1 Responder rates of patients at 4 weeks compared with prevaccinated levels Responder rates of patients at 4 weeks compared with prevaccinated levels.

Figure 1 Proportions of the major B-cell subsets in DMF-treated patients Proportions of the major B-cell subsets in DMF-treated patients B cells were collected.

Figure 1 Flowchart of patient inclusion

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Figure 6 Cellular composition after tissue dissociation

Figure 1 Total IgG, IgA, and IgM levels and hypo-Ig prevalence during RTX treatment Total IgG, IgA, and IgM levels and hypo-Ig prevalence during RTX treatment.

Figure 2 Changes in fatigue under treatment

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

Figure 1 Annualized percentage brain volume change

Figure 2 BVL according to on-study disability worsening

Figure 2 Repopulation of CD19+ cells in low and high BSA patients and calculation of the BSA Repopulation of CD19+ cells in low and high BSA patients and.

Figure 2 Frequency of the proportion of total WMLs with central veins in PPMS, RRMS, and SVD Frequency of the proportion of total WMLs with central veins.

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 DMF promotes an anti-inflammatory cytokine B-cell profile

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Figure Serial brain MRI of the patient with encephalitis and spontaneous recovery accompanying IgLON5 autoimmunity Serial brain MRI of the patient with.

Figure 1 Tissue processing methods and cellular viability

Figure 3 Freedom from clinical disease activity during 36 months of fingolimod treatment Freedom from clinical disease activity during 36 months of fingolimod.

Figure 3 C5B3 blocked MAC formation

Figure 3 Within-group comparisons (before–after)‏

Figure 4 Patient 3 MRI evolution over time

Figure 1 Segmentation of the normal-appearing periependymal white matter Segmentation of the normal-appearing periependymal white matter The figure demonstrates.

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

Figure 3 A receiver operating characteristic curve of days to IVMP as a predictor of failure to regain 0.2 logMAR (20/30) vision (AUC 0.84, p < 0.001)‏

Figure 1 Axial FLAIR brain MRI obtained on admission to the ICU demonstrated (A1) old hyperintense subcortical lesions (arrowhead), new superimposed on.

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.

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Figure 2 Nonhuman primate brain immunohistochemistry Nonhuman primate brain immunohistochemistry (A) Purified IgG-AF594 from patients (A.a) and from controls (A.b). (B) Brain and cerebellum nonhuman primate myelin staining with commercial monoclonal MOG 8–18C5. (C) Purified IgG-AF594 from patients colocalized with commercial anti-MBP. An example of patient Id.1. hMOG = human MOG; MBP = myelin basic protein; MOG = myelin oligodendrocyte glycoprotein; NHP = nonhuman primate. Alvaro Cobo-Calvo et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e543 Copyright © 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.