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.

Slides:

Advertisements

Similar presentations

Figure 2 ERG amplitude reduction in the follow-up study

Advertisements

Figure 1 Box plot of the venous diameter in lesions

Figure 1 Regional changes in FA values

Figure 2 GlyR antibody binding

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 2 Spinal cord lesions

Figure 2 Serums of patients with stiff-person syndrome spectrum disorders containing GlyRα1-Binding IgG specifically induces internalization of GlyRα1.

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

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 2 The frequency of helper T cells (Th) within CD4+ population and TCRγδ within CD3+ cells is affected by FTY and DMF treatment The frequency of.

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

Figure 1 Histopathologic features of case 1 (A–G) and case 2 (H–L)‏

Figure 1 The abundance of CD3+ T cells and their subtypes are significantly affected by FTY and DMF treatment The abundance of CD3+ T cells and their subtypes.

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 2 Histopathologic findings of patients with both inflammatory myopathy and myasthenia gravis Histopathologic findings of patients with both inflammatory.

Figure 3 Temporal trends in FALS incidence

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 3 Receiver operating characteristics for CSF glucose (n = 225) and serum/CSF glucose ratio (n = 156) as predictors for microbial meningitis Receiver.

Figure 1 Characteristics of the German National MS Cohort

Figure 2 Linkage analysis of chromosome 19

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

Figure 3 Analysis of the prognostic value of IL-10–producing B cells or IL-6/IL-10–B-cell ratio measurements in patients with RIS/CIS MS Analysis of the.

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 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 1 Phenotype and functional properties of B cells in MS and HCs at baseline Phenotype and functional properties of B cells in MS and HCs at baseline.

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 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 6 Cellular composition after tissue dissociation

Figure 2 Immunohistological detection of EBV latent and early lytic proteins in MS and control brains Immunohistological detection of EBV latent and early.

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 3 Muscle biopsy showing myofiber atrophy and degeneration

Figure 1 bvFTD PINBPA network

Figure 2 Seizure outcomes

Figure 2 Overview of apheresis therapies

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

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

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

Figure 1 Tissue processing methods and cellular viability

Figure 3 C5B3 blocked MAC formation

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 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

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 2 Correlations of subcortical gray matter SUVRs with the EDSS score, T25FW, and BPV in MS Correlations of subcortical gray matter SUVRs with the.

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.

Presentation transcript:

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 binding to AQP4 (A) After incubation with 10% serumNMOSD and 2.5% hC with or without C5B3, C3A6, and C5B35, we measured CHO cells cytotoxicity with LIVE/DEAD staining. (B) The percentage of dead cells from the experiments shown in Fig A. (C.a) CDC in M23-AQP4–overexpressing CHO cells incubated with 2.5% hC and different concentrations of serumNMOSD and C5B3. (C.b) CDC in M23-AQP4–overexpressing CHO cells incubated with 10% serumNMOSD and different concentrations of hC and C5B3. (D) We fixed the CHO cells and incubated them with 10% serumNMOSD with and without 800 μg/mL of C5B3 for immunostaining of AQP4 (red) and human IgG (green). The scale bar size for both A and D stains are all 200 μm. ***p < 0.001. AQP4 = aquaporin-4; CDC = complement-dependent cytotoxicity; hC = human complement; IgG = immunoglobulin G. Wenli Zhu et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e561 Copyright © 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.