Figure 4 Expression of type 1 IFN cytokines in different aDM subtypes

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Figure Pedigrees of the SCA42 families identified in this study

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Figure Comparative myopathology of immune myopathies with perimysial pathology (IMPP) and dermatomyositis with vascular pathology (DM-VP)‏ Comparative.

Figure 1 Box plot of the venous diameter in lesions

Figure 2 Needle biopsy of the left vastus lateralis

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 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 Neuroimaging and pathology

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 Facial photograph during headache attack and brain and upper cervical cord MRI Facial photograph during headache attack and brain and upper cervical.

Figure 2 Anti-LINGO-1 (Li81) does not affect cytokine production

Figure 5 IM amplification loop of type 1 IFN-inducible gene expression

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 3 Decreased AHI1 in human CD4+ T cells is associated with decreased proliferation and increased IFNγ production Decreased AHI1 in human CD4+ T cells.

Figure Muscle biopsy of the left biceps showing the characteristic pathologic findings in BCIM Muscle biopsy of the left biceps showing the characteristic.

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

Figure 3 Age, pretreatment, sex, and leukopenia do not influence CD19+ cell repopulation Age, pretreatment, sex, and leukopenia do not influence CD19+

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 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 3 Morphologic and molecular analyses of B-cell infiltration and ELS formation in DM Morphologic and molecular analyses of B-cell infiltration and.

Figure 2 Histopathologic evaluation of sections of muscle biopsy specimens based on 4 different domains Histopathologic evaluation of sections of muscle.

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 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 1 Sections of muscle biopsy specimens stained with hematoxylin & eosin (HE)‏ Sections of muscle biopsy specimens stained with hematoxylin & eosin.

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 Mutation carrier–derived lymphoblastoid cell lines (LCLs) show decreased aconitase 2 activity and mitochondrial respiration deficiency compared.

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.

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Figure 1 Family pedigree and DNA sequencing results

Figure 4 Leukocyte subset isolation from brain tissue by enzymatic dissociation Leukocyte subset isolation from brain tissue by enzymatic dissociation.

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

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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 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 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.

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

Figure 3 Muscle biopsy showing myofiber atrophy and degeneration

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Figure 1 Analysis of inflammatory cells in muscle biopsies

Figure 1 MRIs (case 1)‏ MRIs (case 1) An enlarging T2 lesion in the cerebral white matter near the angular gyrus and a new lesion in the left middle cerebellar.

Figure 2 MRIs (cases 2 and 3)‏

Figure 3 C5B3 blocked MAC formation

Figure 3 Within-group comparisons (before–after)‏

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 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)‏

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Figure 1 Glutamine antagonist JHU083 inhibits T-cell proliferation in vitro Glutamine antagonist JHU083 inhibits T-cell proliferation in vitro T-cell proliferation.

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Figure 4 Expression of type 1 IFN cytokines in different aDM subtypes Expression of type 1 IFN cytokines in different aDM subtypes CD23+ B cells are a source of CXCL13 as indicated by double immunofluorescent staining (A, arrowheads). Gene expression of CXCL12 and CXCL13 was illustrated by the log10 of fold change values compared with the normal controls. Results show mean ± SEM. *p < 0.05, **p < 0.01. (B) EM revealed tubuloreticular inclusions (arrowheads) in the cytoplasm of a B-lymphocyte (solid and dashed boxes indicate magnified areas; * = mitochondrion). MxA staining revealed strong expression in the perifascicular area on myofibers and capillaries (C, arrows) in all cases and additional expression by B cells in B-cell–rich and follicle-like aDM (C, arrowheads). In contrast to healthy controls, muscle fibers of different DM subgroups showed upregulation of ISG20 (D; CRTL: normal control). aDM = adult dermatomyositis; DM = dermatomyositis; IFN = interferon; IM = intramuscular; ISG = interferon-stimulated gene; MxA = myxovirus resistance gene A; n = nucleus. Josefine Radke et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e451 Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.