Gene expression of CD4+CD8+ Tfh cells in lesions of IgG4-related disease and CD4+CD8+ Tfh in tonsil.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE202617 | GEO | 2022/08/10
REPOSITORIES: GEO
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Project description:To address a possible role of Tfh (CD3+CD4+CXCR5hiPD-1hi) cells in IgG4-related disease(IgG4-RD), we investigated Tfh cells as well as other lymphocyte subsets residing within the affected tissue lesions of IgG4-RD in this study. When compared to gene expression profiles of Tfh cells within tonsils, inflammatory lesions in IgG4-RD preferentially contained Tfh cells with the expression of signature genes of cytotoxic T lymphocytes. Whereas the expression levels of Tfh-related genes like IL-21, CD200, and Pou2af1 (also named as Bob1) in GC-type Tfh cells of IgG4-RD seemed to be relatively lower than those of GC-type Tfh cells within tonsils. GC-type Tfh cells of IgG4-RD expressed low levels of genes related to Th2 cells, Th17 cells, and Treg cells, albeit the genes related to Th1 cells and interaction of T cells and B cells.
2022-08-10 | GSE202615 | GEO
Project description:To understand physiological characteristics of CD4+CD8+ Double-positive (DP)-Tfh cells, we continued to conduct comparative transcriptome analysis of tonsillar Tfh cell populations, including DP-Tfh cells and CD4+CD8- single-positive (SP)-Tfh cells as a control. Results showed that DP-Tfh cells preferentially expressed transcripts related to CTLs, such as CD8 (CD8A and CD8B), Eomes, and granzymes, suggesting a possible cytotoxic attribute of DP-Tfh cells. Th1-cell related signature genes were also presented in DP-Tfh cells and cytokines like interferon (IFN)-gamma and interleukin (IL)-10 were found to be highly presented in DP-Tfh cells rather than SP-Tfh cells. Of note, the expression profile of authentic Tfh-cell (i.e. SP-Tfh cell) related genes like IL-4, IL-21, Bcl6, and Pou2af1 seemed to be shared with DP-Tfh cells.
2022-08-10 | GSE202616 | GEO
Project description:Immunoglobulin G4 (IgG4)-related disease (IgG4-RD) is a fibroinflammatory disorder signified by aberrant infiltration of IgG4-restricted plasma cells in a variety of organs. Clinical presentation is heterogeneous and pathophysiological mechanisms of IgG4-related autoimmunity remain elusive. Secondary parenchymal lesions of IgG4-RD in the central nervous system (CNS) are rare and there are very few cases of IgG4-RD with isolated CNS manifestation. Patients suffering from IgG4-RD frequently require prolonged treatment with glucocorticoids and are often unable to taper these medications. By leveraging single-cell sequencing of the cerebrospinal fluid (CSF) of a patient with an unusual inflammatory intracranial pseudotumor we provide novel insights into the immuno-pathophysiology of IgG4-RD by illustrating an IgG4-RD-associated polyclonal T cell response in the CSF and multifaceted cell-cell interaction between immune cell subsets and pathogenic B cells.
2021-06-19 | E-MTAB-10479 | biostudies-arrayexpress
Project description:In this experiment we generated Affymetrix gene expression data for T Follicular Helper (TFH) cells from tonsils of healthy volunteers (4 biological replicates) and naive CD4-positive helper T cells (2 biological replicates). TFH cells provide a model relevant to SLE as TFH operate upstream of the activation of pathogenic autoantibody-producing B cells during the disease. This experiment accompanies promoter capture-C and ATAC-seq experiments on the same cell types.
2019-04-01 | E-MTAB-6637 | biostudies-arrayexpress
Project description:<Objective> To compare gene expression in labial salivary glands (LSG) of IgG4-related disease (IgG4-RD) with SjM-CM-6grenM-bM-^@M-^Ys syndrome (SS). <Methods> Gene expression was analyzed by DNA microarray in LSG of IgG4-RD (n=5), SS (n=5), and healthy controls (n=3). Differentially expressed genes (DEGs) in IgG4-RD and SS were identified, and gene-annotation enrichment analysis of these DEGs was performed using Gene Ontology (GO) annotation. Validation of the result was performed by quantitative PCR using LSG from IgG4-RD (n=9), SS (n=10), and controls (n=4). <Results> Gene expression patterns in IgG4-RD, SS, and healthy controls were quite different with each other in hierarchical clustering as well as principal component analysis. In IgG4-RD, 1771 up-regulated probe sets (corresponding to 1321 up-regulated genes) and 1785 down-regulated probe sets (corresponding to 1320 down-regulated genes) were identified as DEGs (false discovery rate <0.05). GO term analysis indicated that the up-regulated set of DEGs in IgG4-RD encoded proteins that function in cell proliferation, extracellular matrix organization, and organ development. PCR validated significantly higher expression of lactotransferrin (LTF) in IgG4-RD than SS (P<0.05), and chemokine (C-C motif) ligand 18 (CCL18) in IgG4-RD than SS and controls (P<0.05). <Conclusion> The results clearly showed that the gene expression pattern in LSG of IgG4-RD is different from that of SS. LSG samples were collected from 5 Japanese patients with IgG4-RD, as well as from 5 Japanese patients with SS who had been followed up at University of Tsukuba Hospital (Ibaraki, Japan). All patients with IgG4-RD satisfied the comprehensive diagnostic criteria for IgG4-related disease (IgG4-RD) 2011 proposed by the All Japan IgG4 team [3]. The diagnosis of IgG4-RD was based on the presence of all three items; 1) clinical examination showing characteristic diffuse/localized swelling or masses in single or multiple organs, 2) Hematological examination shows elevated serum IgG4 concentrations (135 mg/dl), 3) Histopathologic examination shows: (1) Marked lymphocyte and plasmacyte infiltration and fibrosis. (2) Infiltration of IgG4+ plasma cells: ratio of IgG4+/IgG+ cells > 40% and >10 IgG4+ plasma cells/HPF. All patients with SS satisfied the Japanese Ministry of Health criteria for the diagnosis of SS (1999) [4]. These criteria included four clinicopathological findings: lymphocytic infiltration of the salivary or lacrimal glands, dysfunction of salivary secretion, keratoconjunctivitis sicca, and presence of anti-SS-A or SS-B antibodies. The diagnosis of SS was based on the presence of two or more of the above four items. Approval for this study was obtained from the local ethics committee and a signed informed consent was obtained from each subject.
2014-06-23 | E-GEOD-40568 | biostudies-arrayexpress
Project description:Transcriptome analysis in patients with IgG4-RD and healthy controls IgG4-related disease (IgG4-RD) is a new emerging disease entity characterized by elevated serum IgG4 concentrations and tissue tumefaction or infiltration by IgG4-positive plasma cells. At present, however, it is not clear whether IgG4-RD is caused by abnormalities in acquired immunity, like autoimmune diseases, or whether the excess production of IgG4 is a true cause of IgG4-RD or an epiphenomenon associated with inflammatory and/or allergic reactions. We therefore attempted to identify genes related to the pathogenesis or clinicopathology of IgG4-RD. Peripheral blood mononuclear cells (PBMCs) were obtained from patients with IgG4-RD before and after steroid therapy and from healthy controls. Total RNA was extracted and DNA microarray analysis was performed to screen for genes showing changes in expression.
2015-03-03 | GSE66465 | GEO
Project description:IgG4-related disease (IgG4-RD) is an autoimmune disease with an unknown etiology. In this study, we focused on non-hematopoietic cells in the submandibular gland of IgG4-RD patients. Through single-cell RNA sequencing, our aim was to unravel the contributions of these cells to the development and progression of IgG4-RD.
2024-02-19 | GSE242778 | GEO
Project description:Transcriptome analysis in patients with IgG4-RD and healthy controls IgG4-related disease (IgG4-RD) is a new emerging disease entity characterized by elevated serum IgG4 concentrations and tissue tumefaction or infiltration by IgG4-positive plasma cells. At present, however, it is not clear whether IgG4-RD is caused by abnormalities in acquired immunity, like autoimmune diseases, or whether the excess production of IgG4 is a true cause of IgG4-RD or an epiphenomenon associated with inflammatory and/or allergic reactions. We therefore attempted to identify genes related to the pathogenesis or clinicopathology of IgG4-RD. Peripheral blood mononuclear cells (PBMCs) were obtained from patients with IgG4-RD before and after steroid therapy and from healthy controls. Total RNA was extracted and DNA microarray analysis was performed to screen for genes showing changes in expression. To exclude any gender-related differences in gene expression, DNA microarray analysis was performed only on samples obtained from male patients and controls. Total RNA was reverse transcribed to cDNA using AmbionM-BM-. WT Expression kits (Applied Biosystems, Foster City, CA), labeled with GeneChipM-BM-. WT Terminal Labeling and Controls kits (Affymetrix, Santa Clara, CA), and hybridized to GeneChipM-BM-. Human Gene 1.0 ST Arrays (Affymetrix), which include 28869 probes. Digitalized image data were processed using GeneChipM-BM-. Operating Software (Affymetrix).
2015-03-03 | E-GEOD-66465 | biostudies-arrayexpress
Project description:<Objective> To compare gene expression in labial salivary glands (LSG) of IgG4-related disease (IgG4-RD) with Sjögren’s syndrome (SS). <Methods> Gene expression was analyzed by DNA microarray in LSG of IgG4-RD (n=5), SS (n=5), and healthy controls (n=3). Differentially expressed genes (DEGs) in IgG4-RD and SS were identified, and gene-annotation enrichment analysis of these DEGs was performed using Gene Ontology (GO) annotation. Validation of the result was performed by quantitative PCR using LSG from IgG4-RD (n=9), SS (n=10), and controls (n=4). <Results> Gene expression patterns in IgG4-RD, SS, and healthy controls were quite different with each other in hierarchical clustering as well as principal component analysis. In IgG4-RD, 1771 up-regulated probe sets (corresponding to 1321 up-regulated genes) and 1785 down-regulated probe sets (corresponding to 1320 down-regulated genes) were identified as DEGs (false discovery rate <0.05). GO term analysis indicated that the up-regulated set of DEGs in IgG4-RD encoded proteins that function in cell proliferation, extracellular matrix organization, and organ development. PCR validated significantly higher expression of lactotransferrin (LTF) in IgG4-RD than SS (P<0.05), and chemokine (C-C motif) ligand 18 (CCL18) in IgG4-RD than SS and controls (P<0.05). <Conclusion> The results clearly showed that the gene expression pattern in LSG of IgG4-RD is different from that of SS.
2014-06-23 | GSE40568 | GEO
Project description:CD4 T cell help is critical for both the generation and maintenance of germinal centers, and T follicular helper (TFH) cells are the CD4 T cell subset required for this process. SAP (SH2D1A) expression in CD4 T cells is essential for germinal center development. However, SAP-deficient mice have only a moderate defect in TFH differentiation as defined by common TFH surface markers. CXCR5+ TFH cells are found within the germinal center as well as along the boundary regions of T/B cell zones. Here we show that germinal center associated T cells (GC TFH) can be identified by their co-expression of CXCR5 and the GL7 epitope, allowing for phenotypic and functional analysis of TFH and GC TFH populations. Here we show GC TFH are a functionally discrete subset of further polarized TFH cells, with enhanced B cell help capacity and a specialized ability to produce IL-4 in a TH2-independent manner. Strikingly, SAP-deficient mice have an absence of the GC TFH subset and SAP- TFH are defective in IL-4 and IL-21 production. We further demonstrate that SLAM (Slamf1, CD150), a surface receptor that utilizes SAP signaling, is specifically required for IL-4 production by GC TFH. GC TFH cells require IL-4 and IL-21 production for optimal help to B cells. These data illustrate complexities of SAP-dependent SLAM family receptor signaling, revealing a prominent role for SLAM receptor ligation in IL-4 production by germinal center CD4 T cells but not in TFH and GC TFH differentiation. Analysis of in vivo antigen-specific (LCMV-specific, SMARTA TCR transgenic) WT and Sh2d1a-/- follicular helper CD4 T cells (CXCR5high),versus non-follicular helper CD4 T cells (CXCR5low), eight days after viral infection.
2010-04-28 | E-GEOD-21379 | biostudies-arrayexpress