Figure 2 B cell development, tolerance checkpoints, and neuromyelitis optica immunotherapy Antibodies are generated during early B cell development by.

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Lymphocyte Development & Generation of Lymphocyte Antigen Receptors Pin Ling ( 凌 斌 ), Ph.D. ext 5632; References: 1. Abbas, A,
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Chapter 10 B-Cell Development
Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.
Figure 2 Proposed model of therapeutic mechanisms of AHSCT
Figure 1 Percent positivity by clinical feature Overall, 6
Figure 2 Anti-LINGO-1 (Li81) does not affect cytokine production
Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.
Proceedings from the National Cancer Institute's Second International Workshop on the Biology, Prevention, and Treatment of Relapse after Hematopoietic.
Figure 3 Decreased AHI1 in human CD4+ T cells is associated with decreased proliferation and increased IFNγ production Decreased AHI1 in human CD4+ T cells.
Nat. Rev. Neurol. doi: /nrneurol
Figure Immune checkpoint inhibitor–induced encephalitis before and after treatment with natalizumab Immune checkpoint inhibitor–induced encephalitis before.
Figure 3 Multifocal visual-evoked potentials in optic neuritis Figure shows the visual-evoked potentials (VEPs) in 52 sectors of the retina. Multifocal.
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 1 Integrative model of NMO/SD pathogenesis
Figure 2 Elevated antibody reactivities against myelin and Epstein-Barr virus (EBV) peptides in relapsing-remitting multiple sclerosis (RRMS) and higher.
Figure 1 MOR103 sequential-dose trial flowchart of study population with multiple sclerosis aPatients received 2 doses of study drug before trial withdrawal.
Figure 3 Gene expression in CSF cell pellets
Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer
Figure 1 Peripheral blood leukocyte subset counts during dimethyl fumarate treatmentComplete blood cell counts were obtained at baseline (n = 34) and at.
Figure 2 DTI values between the hepatitis C group and controls(A) DTI FA values, (B) DTI diffusion values. *Statistically significant at FDR-adjusted p.
Figure 2 Representative brain MRIs from patients with neuromyelitis optica Lesions are localized at sites of high aquaporin-4 expression (white dots).
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 3 Hypothesized cellular and molecular crosstalk influencing NMO/SD Hypothesized cellular and molecular crosstalk influencing NMO/SD (A) Theoretical.
Stages of B-cell development and expression of B-cell surface markers.
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 4 Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis.
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 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 6 Cellular composition after tissue dissociation
Figure 2 Flu immunization–induced changes in the proportions and absolute numbers of B cells and their relevant subpopulations Flu immunization–induced.
Figure 1 Examples illustrating gating strategy for fluorescence-activated cell sorting (FACS)‏ Examples illustrating gating strategy for fluorescence-activated.
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 Central B cell tolerance is compromised in patients with NMOSD. Recombinant antibodies (rIgGs) derived from ... Figure 1 Central B cell tolerance.
Figure 2 Induced deletion of CXCR2 on oligodendrocyte lineage cells after tamoxifen injection in Cxcr2-cKO mice Induced deletion of CXCR2 on oligodendrocyte.
Figure 1 Examination of MuSK antibody levels and B-cell subsetsFlow cytometric analysis (n = 13) using standardized Human Immunology Project Consortium.
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 1 Representative spinal cord MRIs from patients with neuromyelitis optica Longitudinally extensive transverse myelitis of the cervical (A) and cervicothoracic.
Figure 2 Changes in fatigue under treatment
Figure 2 Assessment of systemic disease activityTc99 scintigraphy (A) and fluorodeoxyglucose PET imaging (B, C) at disease onset 2 years before acute deterioration.
Figure 1 Distinct cognitive performers present differences in the cell populations of the adaptive immune systemThe profile (cell counts per mL of blood)
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 3 Flu immunization–induced changes in the proportions and absolute numbers of RORγt-expressing CD4+ and CD8+ T cells Flu immunization–induced changes.
Figure 1 Full-length MOG cell-based assay using a serum dilution of 1:160 as a cutoff for positivity (red line in both plots)(A) Myelin olidgodendrocyte.
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 3 Effect of IVIg on endogenous relative concentration (in mAb equivalents) of JCV AbSix patients shown in this figure have had John Cunningham virus.
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 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 Fluorescence-activated cell sorting (FACS) employing cells singly transfected with M1-AQP4 or M23-AQP4 or cotransfected with both AQP4 isoforms.
Figure 1 Classical pathway and lectin pathway activity in patients with multifocal motor neuropathy and controls Classical pathway (CP) activity (A) and.
Figure 2 Detection of atypical anti-neuronal antibodies Immunohistofluorescence assay on rat brain sagittal slices incubated with the patient's CSF 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.
Figure 2 Cell-based assay demonstrating differential binding of AChR antibodies to the adult and fetal receptorsThe fetal (gamma subunit specific) and.
Gitanjali Das et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e453
Figure 3 Alemtuzumab-induced changes in monocytes
Figure 4 Cell count of selective immune cell subpopulations during alemtuzumab Cell count of selective immune cell subpopulations during alemtuzumab Absolute.
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 1 Numbers/seropositivity rates of IVIg-naive and IVIg-exposed STRATIFY-2 enrollees* = % of enrollment samples, ** = date of IVIg and/or concentration.
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 Longitudinal analysis of peripheral immune cell composition Frequency of naive, central memory (Tcm), and effector memory (Tem) CD4 T cells over.
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Figure 2 B cell development, tolerance checkpoints, and neuromyelitis optica immunotherapy Antibodies are generated during early B cell development by random joining of immunoglobulin gene segments. B cell development, tolerance checkpoints, and neuromyelitis optica immunotherapy Antibodies are generated during early B cell development by random joining of immunoglobulin gene segments. The arbitrary joining is the basis for the vast diversity of the B cell repertoire needed for complete immunity, but this comes at a price: the developing B cell repertoire includes autoreactive antibodies. B cell tolerance ensures that potentially detrimental autoreactive B cells are cleared from the B cell repertoire. During B cell development, autoreactive B cells are removed at 2 separate steps. In the first, a central checkpoint in the bone marrow prior to the transition to immature B cells removes the large portion of developing B cells that express polyreactive antibodies, leaving a smaller fraction of clones with low levels of polyreactivity to migrate from the bone marrow to the periphery. The second tolerance checkpoint, residing in the periphery, further counterselects autoreactive new emigrant B cells before they differentiate into mature naïve B cells. B cell lineages that may be directly affected by potential neuromyelitis optica treatment modalities are shown in the row below the schematic. Surface markers indicated in the bottom part of the schematic are not intended to be comprehensive and do not include all reported subsets. Adapted by permission from Macmillan Publishers Ltd: Nature Immunology (Meffre E, Casellas R, Nussenzweig MC. Antibody regulation of B cell development. 2000;1:379–385). Jeffrey L. Bennett et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e104 © 2015 American Academy of Neurology