Figure 1 The human adaptive immune profile in multiple sclerosis (MS)‏

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Date of download: 7/10/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Altered CD4+/CD8+ T-Cell Ratios in Cerebrospinal.

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Figure 2 ERG amplitude reduction in the follow-up study

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

Figure 3 Antibodies to MOG using different secondary antibodies: Anti-human IgG (H + L), IgG1, or IgM(A) Comparison of binding to full-length myelin oligodendrocyte.

Figure 4 Relation of neuropsychological deficits and intrathecal immune cell subsets in GABAB receptor antibody–associated limbic encephalitis Relation.

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 Differentiation and functional control of T-cell subsets

Figure 3 JCV index changes in JCV+ patients

Figure 2 Comparative milestones in T and B lymphocyte maturation

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

Figure 2 Brain-infiltrating immune cells mainly consist of CD8+ memory T cells Immunofluorescence staining of brain-infiltrating immune cells. Brain-infiltrating.

Figure 1 Effect of DMF therapy on T cell subsets

Figure 2 Alemtuzumab-induced changes in the dendritic cell compartment

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 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 1 Peripheral blood leukocyte subset counts during dimethyl fumarate treatmentComplete blood cell counts were obtained at baseline (n = 34) and at.

Figure 3 Effects of RTX on specific anti-pathogen IgGs

Figure 2. ROC curves for different group comparisons

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 5 Alemtuzumab-induced changes in the innate lymphoid cell (ILC) compartment Alemtuzumab-induced changes in the innate lymphoid cell (ILC) compartment.

Figure 3 Cladogram indicating the effect of disease-modifying therapies on the phylogenetic structure of MS patients' microbiota Cladogram indicating the.

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

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

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 2 Reduced frequency of central memory CD4 T cells in patients with PML Reduced frequency of central memory CD4 T cells (CD4Tcm) (p < ), naive.

Figure 5 Autopsy Mycoplasma DNA analysis

Figure 3 Cytokine gene expression in PBMC stimulated with PPD or MBP in vitroCytokine messenger RNA transcripts were isolated from peripheral blood mononuclear.

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

Figure 1 Association between serum levels of IL-18 and hippocampal volume in patients with schizophrenia Scatter plots show a positive correlation between.

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

Figure 1 Anti-Epstein-Barr virus nuclear antigen-1 IgG quartile antibody status differences in MRI measures Anti-Epstein-Barr virus nuclear antigen-1 IgG.

Figure 2 Peripheral blood lymphocyte subset counts during dimethyl fumarate treatment(A) Lymphocyte subsets were obtained at baseline (n = 21) and at month.

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 1 Examination of MuSK antibody levels and B-cell subsetsFlow cytometric analysis (n = 13) using standardized Human Immunology Project Consortium.

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

Figure 1 CD52 expression on innate myeloid and lymphoid cell subsets

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

Figure 1 Distinct cognitive performers present differences in the cell populations of the adaptive immune systemThe profile (cell counts per mL of blood)

Figure 1. Heat map of antibody binding patterns to glycolipid targets in Guillain-Barré syndrome (GBS) cases and controls Heat map of antibody binding.

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

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 3 DMF promotes an anti-inflammatory cytokine B-cell profile

Figure 2 Assessment of fluctuation in fatigue scores using environmental data The relationship between fatigue (as measured by the Modified Fatigue Impact.

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 2 B-cell very late antigen-4 (VLA-4) deficiency reduced CNS accumulation of B cells, but not proinflammatory or regulatory T cells (Treg), in myelin.

Figure 2 Effect of DMF therapy on the T helper cell repertoire and cytokine production Effect of DMF therapy on the T helper cell repertoire and cytokine.

Figure 4 Vα7.2 TCR chain repertoire Analysis of the T-cell receptor (TCR) Vα7.2 repertoire of patient A by pyrosequencing shows oligoclonal T-cell expansions.

Figure 3 Alemtuzumab-induced changes in monocytes

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 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 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 1 The human adaptive immune profile in multiple sclerosis (MS)‏ The human adaptive immune profile in multiple sclerosis (MS) In A and B, the right upper half, above the diagonal, indicates coregulation between pairs of cell types in healthy controls (n = 36) (red: positive correlation coefficient, blue: negative correlation coefficient, light gray: no data available). Unbiased clustering of coefficients was performed to group coregulated cell types. Upon clustering, a main distinct naive cluster was observed, consisting of coregulated CD4+ T cells, CD4+/CD8+ ratio, and naive T cells, together with recent thymic emigrants (RTE) of both CD4+ and CD8+ lineages. This naive cluster was negatively correlated with activated and antigen-experienced lymphocyte subsets. Several microclusters were additionally observed, with coregulation of regulatory T cells (Tregs) with central memory CD4+ and CD8+ T cells (the antigen-experienced microcluster), coregulation of Th1 cells and interferon-γ-producing CD8+ cells (the Th1 microcluster), coregulation of Th2 and memory B cells (the Th2 microcluster), and so forth, revealing the emergence of known immunologic interactions through this systems immunology approach. In the lower left half, below the diagonal, dark gray indicates coregulation between pairs of cell types in (A) patients with untreated MS (MS_UNT, n = 56) and (B) patients with autoimmune thyroid disease (AITD, n = 55) that does not differ significantly from healthy controls. Coregulation between pairs of cell types that is significantly altered by disease (p < 0.05, and boxed if p < 0.01) in (A) untreated patients with MS vs controls and (B) patients with AITD vs controls is colored (red: positive correlation coefficient, blue: negative correlation coefficient, light gray: no data available). James Dooley et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e240 © 2016 American Academy of Neurology