Figure 3 Multiple sclerosis (MS) immunomodulatory treatments interferon-β (IFNB) and fingolimod (FTY720) result in global perturbation of the immune system.

Slides:

Advertisements

Similar presentations

Copyright © 2011 American Medical Association. All rights reserved.

Advertisements

Figure 2 ALSFRS-R changes (A) Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) slope after 6 months of treatment without (left)

Figure 2. Infliximab treatment effect

Figure 3 B-cell amount and the frequency of various B-cell subtypes are differentially affected by FTY or DMF treatment B-cell amount and the frequency.

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 5 Treatment with fingolimod raises the activation threshold of monocytes in MS Peripheral blood mononuclear cells from 8 healthy donors, 7 patients.

Figure 3 JCV index changes in JCV+ patients

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

Figure 4 Abundance of cytokines which showed significant difference in expression in the plasma and the cultured PBMC of patients with RRMS Abundance of.

Figure 2 Elevated antibody reactivities against myelin and Epstein-Barr virus (EBV) peptides in relapsing-remitting multiple sclerosis (RRMS) and higher.

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 1 MOR103 sequential-dose trial flowchart of study population with multiple sclerosis aPatients received 2 doses of study drug before trial withdrawal.

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

Figure 1 8-Iso-PGF2α levels in CSF of patients with MS and controlsCSF 8-iso-prostaglandin F2α (8-iso-PGF2α) levels were estimated using an ELISA. (A)

Figure 2 Forest plots for subgroup analyses

Figure 1 Time points of blood sampling

Figure 3 Responder subset (A) Percentage of “responders” (nonprogressing patients) at week 25 after 6 months of treatment; percentage of “responders” in.

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 1 Schematic overview of flow cytometry Schematic overview on the analysis of peripheral immune cells by flow cytometry. Schematic overview of flow.

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 The human adaptive immune profile in multiple sclerosis (MS)‏

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 5 Increased B cell-activating factor (BAFF) levels are shared between immunomodulatory treatments Increased B cell-activating factor (BAFF) levels.

Figure 1 JCV serostatus JCV serostatus (A) Serostatus of 1,921 natalizumab-treated patients with multiple sclerosis, with JCV− patients shown in black.

Figure 5 Pairwise correlations between selected patient-reported outcomes and performance tests in patients with MS (A) The number of pairwise correlations.

Figure 3 Longitudinal performance of 2 MS–cohabitant participant pairs on Ishihara color testing Both response speed and response accuracy are provided.

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 2 Overall community differences in the gut microbiota of treated or untreated patients with MS Overall community differences in the gut microbiota.

Figure 4 Shared and unique immune changes induced by multiple sclerosis (MS) immunomodulatory treatments Shared and unique immune changes induced by multiple.

Figure 1. Antibodies to MOG in a proportion of adult patients with MS

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 2 Distinct changes to immunoprofile in autoimmune thyroid disease (AITD) and multiple sclerosis (MS)‏ Distinct changes to immunoprofile in autoimmune.

Figure 3 Correlation of lipid indexes to MRI measures of disease severity in multiple sclerosis Correlation of lipid indexes to MRI measures of disease.

Figure 1 Examples illustrating gating strategy for fluorescence-activated cell sorting (FACS)‏ Examples illustrating gating strategy for fluorescence-activated.

Figure 2 Spectrum of abnormal CT scanning of patients with bacterial meningitis presenting with a minimal Glasgow Coma Scale score Spectrum of abnormal.

Figure 1 BG-12 treatment reduced total circulating B cells and had variable effects on memory B cells BG-12 treatment reduced total circulating B cells.

Figure 2 Correlation of CSF 8-iso-PGF2α levels with other indicators of oxidative stressCorrelations of 8-iso-prostaglandin F2α (8-iso-PGF2α) values with.

Figure 1 Patterns of study retention The proportion of individuals actively participating in the study is displayed over the course of the study. Patterns.

Figure 4 Alemtuzumab-mediated effects on interleukin (IL)–23 and granulocyte-macrophage colony-stimulating factor (GM-CSF) production in innate myeloid.

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 3 TRIF deficiency abrogates the immunomodulatory effects of glatiramer acetate treatment on cytokines and experimental autoimmune encephalomyelitis.

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

Figure 1 Levels of miR-150 are elevated in patients with multiple sclerosis (MS) and patients with clinically isolated syndrome (CIS) who convert to MS.

Figure 2 Changes in fatigue under treatment

Figure 2 Correlation between wGRS and age at onset The figure shows the correlation between weighted genetic risk score (wGRS) and age at onset in all.

Figure 4. The N:M ratio is significantly increased in patients with ALS and correlates with disease progression The N:M ratio is significantly increased.

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 1 Volcano plot Peptides (n = 2,260) showing distribution of fold change and statistical significance. Volcano plot Peptides (n = 2,260) showing.

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 2 Glatiramer acetate treatment induced M2 differentiation through a MyD88-independent pathway (A) As described previously,3 M2 monocytes were treated.

Figure 2 Natalizumab increases expression of proinflammatory genes and cytokines by CD49d+ memory CD4 cells Natalizumab increases expression of proinflammatory.

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

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 Assessment of fluctuation in fatigue scores using environmental data The relationship between fatigue (as measured by the Modified Fatigue Impact.

Figure 2 Kaplan-Meier survival curves for the fingolimod cohort In each graph, bottom tertile: solid line; middle tertile: long dashed line; top tertile:

Figure 1. MBP-specific IFN-γ+ but not IL-17+ frequencies are significantly different between patients with MS and HCs MBP-specific IFN-γ+ but not IL-17+

Figure 1 Classical pathway and lectin pathway activity in patients with multifocal motor neuropathy and controls Classical pathway (CP) activity (A) 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.

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

Figure 2 Time from incident ADS event to MS diagnosis

Figure 1 Numbers/seropositivity rates of IVIg-naive and IVIg-exposed STRATIFY-2 enrollees* = % of enrollment samples, ** = date of IVIg and/or concentration.

Figure 2. Percentage of CD16− monocytes in the blood is reduced during disease progression Percentage of CD16− monocytes in the blood is reduced during.

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 4 Illustration of a practice effect by examining longitudinal performance measures in patients with MS and cohabitants (A) Response time for each.

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 3 Multiple sclerosis (MS) immunomodulatory treatments interferon-β (IFNB) and fingolimod (FTY720) result in global perturbation of the immune system Multiple sclerosis (MS) immunomodulatory treatments interferon-β (IFNB) and fingolimod (FTY720) result in global perturbation of the immune system Patients with MS being treated with one of 4 immunomodulatory treatments (GA = glatiramer acetate; NAT = natalizumab) were plotted together with controls (CON) and untreated (UNT) patients with MS using nonparametric multidimensional scaling over 38 immunologic variables. Individual patients and distance from the average of each condition are shown. Variation explained by each axis is indicated in the parentheses. Pairwise distance of samples was calculated based on Bray-Curtis dissimilarity index. James Dooley et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e240 © 2016 American Academy of Neurology