Figure 1 GABAB expression in the thymus(A–C) Staining of thymus tissue with anti-cytokeratin (A) and anti-GABAB antibody (B, C double immunofluorescence).

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Figure 3 Brain MRI findings in patients with MOG-Ab Extensive brain lesions with large diameter (A and B), posterior reversible encephalopathy–like lesions.

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Figure 1 Muscle biopsy from a patient with a slowly progressive (24 years) HMGCR antibody–associated myopathy syndrome (A) Hematoxylin & eosin stain, (B)

Figure 2 GlyR antibody binding

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 Vertebral artery angiogram and tissue pathology

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 3 Immunohistochemical analyses of positive and negative Epstein-Barr virus (EBV) control tissues using immunostaining Immunohistochemical analyses.

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

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

Figure 1 Treg percentage and suppressive function increased during each round of Treg infusions Treg percentage and suppressive function increased during.

Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.

Figure 2 Expression of GABAA receptor and LGI1 by patient's thymomaTissue sections of the patient's thymoma incubated with biotinylated immunoglobulin.

Figure DPPX antibodies as detected by fluorescence-based immunohistochemistry and a cell-based assayImmunohistochemistry displayed binding of the patient's.

Figure. Patient imaging

Figure 1 Reactivity of the patients' antibodies with rat brain and HEK cell-based assays Rat hippocampal dentate gyrus neuropils were stained with patient.

Figure 1 Flow diagram of the assays and the samples that were evaluatedA total of 1,109 samples were initially screened at a serum dilution of 1:20 for.

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

Figure 2 Brain biopsy Brain biopsy (A) Double staining with anti-aquaporin-4 (AQP4) antibody (dark green) and Luxol fast blue (blue) is shown. Loss of.

Figure 1 Cerebral MRI during the disease course Cerebral MRI with multiple cerebral supratentorial lesions during the disease course: periventricular lesions.

Figure 2 APCs from laquinimod-treated mice inhibit differentiation of Tfh cells APCs from laquinimod-treated mice inhibit differentiation of Tfh cells.

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 2 Binding of the patient's IgG to Purkinje cells is inhibited by pretreatment of rat tissue with anti-VGCC antibodies, confirming specificity of.

Figure 2 Overview of the patient's history and immunofluorescence pattern of patient CSF IgG Overview of the patient's history and immunofluorescence pattern.

Figure. Groups 1–3, patients tested, and test results (viral PCR and antibodies)‏ Groups 1–3, patients tested, and test results (viral PCR and antibodies)

Figure 2 CD4+ and CD8+ T cells accumulate in the CSF in GABAB receptor antibody–associated LE CD4+ and CD8+ T cells accumulate in the CSF in GABAB receptor.

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 VGCC antibody uptake in cerebellar slice culture

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

Figure 2 Cerebral and spinal MRI (A) Restricted diffusion of both optic nerves (arrows) on diffusion-weighted and apparent diffusion coefficient imaging.

Figure 2. Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem.

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

Figure 1 B cells and plasma cells accumulate in the CSF in GABAB receptor antibody–associated LE B cells and plasma cells accumulate in the CSF in GABAB.

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 Varicella-zoster virus antigen in the temporal artery, aorta, and carotid artery of a patient with refractory giant cell arteritis Immunohistochemical.

Figure Leptomeningeal inflammationPostcontrast T1-weighted MRI: abnormal leptomeningeal enhancement over the frontoparietal lobes and interhemispheric.

Figure 4 ADP-induced migration of human microglia is blocked by a P2Y12 antagonist(A) Using 10 μm cell migration chambers followed by crystal violet staining,

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

Figure 2 Clinical and autoantibody status of 2 CNTN1 or NF155+ patients not receiving rituximab Despite corticosteroids and methotrexate treatment, patient.

Figure 1 CD52 expression on innate myeloid and lymphoid cell subsets

Figure 1 Determination of anti-Tr/DNER by indirect immunofluorescence(A) Slide with 10 reaction fields as used for the study. Determination of anti-Tr/DNER.

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 1. Spinal cord MRI and immunofluorescence staining of the patient's serum and controls on different tissues and recombinant cell substrates Spinal.

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 Comparison of LC activation in diabetic small fiber neuropathy and normal control(A) PGP9.5 immunostaining shows decreased density of epidermal.

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 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.

Figure 1 Follow-up periods of 33 anti–3-hydroxy-3-methylglutaryl coenzyme A reductase autoantibody (HMGCR Ab+) myopathy patients in relation to cancer.

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.

Figure 6 P2Y12 is highly expressed in CD68+ and CD163+ cells during parasitic brain infectionIn a case of Schistosoma mekongi infection, hematoxylin and.

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

Figure 3. Sensitivity and specificity of microarray analysis in relation to target number Sensitivity and specificity of microarray analysis in relation.

Figure 2 Detection of slanDCs in CSF of patients with MS(A, B) Immunocytochemical stainings were performed to determine the presence of 6-sulfo LacNAc+

Figure 2 Antibodies to MOG detected with anti-human IgG (H + L) as the secondary antibody(A) Schematic of the human MOG proteins tested. Antibodies to.

Figure 4 Cell count of selective immune cell subpopulations during alemtuzumab Cell count of selective immune cell subpopulations during alemtuzumab Absolute.

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. Histoimmunoprecipitation and antigen identification

Figure 3. Verification of GluRd2 as the target antigen of the patient's antineural autoantibodies Verification of GluRd2 as the target antigen of the patient's.

Presentation transcript:

Figure 1 GABAB expression in the thymus(A–C) Staining of thymus tissue with anti-cytokeratin (A) and anti-GABAB antibody (B, C double immunofluorescence). GABAB expression in the thymus(A–C) Staining of thymus tissue with anti-cytokeratin (A) and anti-GABAB antibody (B, C double immunofluorescence). Cytokeratin-positive epithelial cells express GABAB receptor (arrows). In addition, GABAB is expressed in other cell types of the thymus, most likely T cells (arrowheads). (D–F) Staining of thymus tissue with anti-cytokeratin (D) and patient sera (E, F double immunofluorescence). Patient antibodies clearly co-localize with cytokeratin-positive epithelial cells. The pattern of staining and co-localization in these areas is identical to panels A, B, and C. Due to antibody combination and tissue availability restrictions, we were unable to triple stain for cytokeratin-GABAB-serum. From our results it can be safely inferred that the GABAB serum autoantibodies bind GABAB that is expressed in thymic epithelial cells. GABAB = γ-aminobutyric acid receptor B. Harry Alexopoulos et al. Neurol Neuroimmunol Neuroinflamm 2014;1:e39 © 2014 American Academy of Neurology