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.

Slides:

Advertisements

Similar presentations

Figure Pedigrees of the SCA42 families identified in this study

Advertisements

Figure 2 ERG amplitude reduction in the follow-up study

Figure 1 Box plot of the venous diameter in lesions

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 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 1 Hierarchical clustering (HCL) outcome of all tested samples with the expression profile of the case report set as unknown Hierarchical clustering.

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 Immune checkpoint inhibitor–induced encephalitis before and after treatment with natalizumab Immune checkpoint inhibitor–induced encephalitis before.

Figure Pedigree of the family

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

Figure 1 Quantitative spinal cord MRI maps and segmentations

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 3 Effects of RTX on specific anti-pathogen IgGs

Figure 3 Temporal trends in FALS incidence

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 3 Clinical outcome of apheresis therapies for NMOSD attacks

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 MRI of inflammatory myelitis before and after treatment

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

Figure 4 Relative abundances of the order Clostridiales and its family members are differentially changed by therapy Relative abundances of the order Clostridiales.

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 Comparison between minutes of MVPA/day and nDGv in patients with MS (green) or monoADS (blue)‏ Comparison between minutes of MVPA/day and nDGv in.

Table 2 Rs number, gene, OR, 95% CI, and permutation p value for the statistical significant variants resulted from allelic association analysis association.

Figure 1 [18F]florbetapir standardized uptake value ratio analytical method [18F]florbetapir standardized uptake value ratio analytical method Flowchart.

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 Flowchart of patient inclusion

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 1 Histamine flare in patients and controls

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 C5B3 prevented AQP4-IgG–mediated CDC without affecting AQP4-IgG binding to AQP4 C5B3 prevented AQP4-IgG–mediated CDC without affecting AQP4-IgG.

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

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 Within-group comparisons (before–after)‏

Figure 2 Clinical data and variation of sNfL levels of patients 4–6 with ATZ-treated MS Clinical data and variation of sNfL levels of patients 4–6 with.

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 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 EDSS score (A), T2LV (B) and T1LV (C) courses in patients who experienced WNS after FTY withdrawal EDSS score (A), T2LV (B) and T1LV (C) courses.

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 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 IgG, IgA, and IgM levels were measured in 188 samples from 15 patients with NMOSDs treated with RTX. Median follow-up period was 70 (range 17–124) months. Levels of total IgG, IgA, and IgM in all serum samples are represented in panels A, C, and E, respectively. Black lines represent the thresholds defining hypo-IgG (<7.0 g/L), –IgA (<0.7 g/L), and –IgM (<0.4 g/L). In addition, based on augmented infectious risk, severe hypo-IgG was defined as total IgG levels <4.0 g/L and severe hypo-IgM as total IgM levels <0.2 g/L. Long-term RTX treatment reduced the levels of all Ig classes. Statistical analysis was performed using univariate linear mixed models. Panels B, D, and F show the prevalence of hypo-Ig over time according to each specific cutoff. The percentage of patients developing hypo-IgG, hypo-IgA, and hypo-IgM has been calculated in patients with a prolonged follow-up period (≥5 years, n = 7 patients), which showed an increased prevalence over time. In particular, prevalence of patients developing hypo-IgG is represented in panel B: patients developing severe hypo-IgG (IgG < 4g/L) are represented in purple, as patients showing mild hypo-IgG (5 g/L ≤ IgG < 7 g/L) are represented in gray. Prevalence of patients developing hypo-IgA (IgA < 0.7 g/L) is shown in panel D (gray). Prevalence of patients developing hypo-IgM is shown in panel F: patients developing severe hypo-IgM (IgM <0.2 g/L) are represented in purple, as patients showing mild hypo-IgM (0.2 g/L ≤ IgG < 0.4 g/L) are represented in gray. Andrea Marcinnò et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e498 Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.