Gene expression in patient and control T cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE69090 | GEO | 2015/06/01
SECONDARY ACCESSION(S): PRJNA284507
REPOSITORIES: GEO
Similar Datasets
Project description:Recent data indicate that intracellularly activated and autocrine-functioning complement activation fragments - in conjunction with an NLRP3 inflammasome - is critical for normal human Th1 induction and contraction. More specifically, engagement of of the C3aR and CD46 by autocrine generated C3a and C3b, respectively, drives the metabolic reprogramming needed for IFN-gamma secrtion by human CD4+ T cells. It was not clear whether autocrine complement and/or the NLRP3 inflammasome are also needed for normal human cytotoxic CD8+ T cell (CTL) responses. During this study, we used CTLs isolated from patients with either CD46 deficiency or with NLRP3 hyperactivity to determine that CD46 is also required for normal IFN-gamma secretion as well as killing activity in CTLs, whilst a canonical NLRP3 inflammasome is not required for these key functions. The CD46-deficient patient utilized in this study has a mutation in the CD46 gene that leads to reduced cell surface CD46 expression and a dysfunction in Th1 induction. The patient suffers from episodes of atypical hemolytic uremic syndrome (aHUS) and common variable immune deficiency (CVID) and recurrent infections.
2018-09-14 | GSE119913 | GEO
Project description:We performed a comparison of transcriptome between follicular CD8 T cells (CXCR5+CD8+CD3+) from 3 lymph nodes of patients with common variable immunodeficiency (CVID) and 3 tonsils of healthy donors, discovering 67 differentially expressed genes that show immunoregulatory potential of CVID follicular CD8 T cells.
2019-09-27 | GSE138076 | GEO
Project description:In this experiment, we explore if circulating microRNAs are altered in patients with atypical hemolytic uremic syndrome (aHUS). To do so, we analyze 4 different pooled samples of aHUS (Pool 1-4) in the arrays and 2 pools of age and gender-matched control samples (Pool F and Pool M). aHUS pools consist of patients samples with different characteristics regarding the presence of complement gene mutations: Pool 1: patients without identified mutations (n=5) Pool 2: patients with mutations in CFH (n=5) Pool 3: patients with mutations in MCP (n=5) Pool 4: patients with mutations in C3 or CFB (n=5) In the case of the control samples, pool F consists of 10 samples of healthy women and pool M consists of 10 samples of healthy men. In conclusion, circulating miRNAs levels are altered in aHUS compared with controls. This alteration is variable and could be mediated by the presence of the complement genetic defect.
2022-12-31 | E-MTAB-8899 | biostudies-arrayexpress
Project description:Patient-specific iPSC-derived endothelial cells reveal aberrant p38 MAPK signaling in atypical hemolytic uremic syndrome
| PRJNA563529 | ENA
Project description:T cells were collected from four healthy donors using heparin anti-coagulant, diluted with equal amounts of PBS EDTA, then layered over Lymphoprep and spun to collect PBMCs. CD4+ T cells were purifed using the Miltenyi positive selection magnetic labeling kit. Cells were resuspended in RPMI (Invitrogen) with 10% FCS amd 50 U/ml IL-2 (Immunotools), and 3.5x105 plated out per well in 48 well plates, coated overnight with 2 µg/ml anti-CD3 and either anti-CD28 or anti-CD46. Purity was assessed by flow cytometry and was in all cases ⥠95%. RNA was purified from a set of unactivated cells before plating, to represent the resting, 0 hr time point samples. For early activation samples, CD28 or CD46 co-stimulated cells were harvested 2 hrs after plating. Then, 36 hours after plating, the remaining CD46-stimulated cells were harvested and labeled for IL-10 or IFN-g secretion using the Miltenyi cytokine detection kits, according to manufacturerâs instructions. Cells were then sorted into separate cytokine-secreting populations (IFN-g+/IL-10â, IFN-g+/IL-10+, and IFN-gâ/IL-10+) using a BD biosciences FACS machine.RNA from separate populations was labeled using the Hy3 microRNA (miRNA) Power labeling kit (Exiqon) and hybridised to an LNA (locked nucleic acid)-based miRCURY miRNA microarray slides (Exiqon, version 11) using a Maui hybridisation chamber (BioMicrosystems). Spot signals were acquired with an Agilent array scanner and GenePix Pro 4.1 was used for annotation (mirBase 14.0), signal processing and quantification using default background subtraction.
2016-07-03 | E-MTAB-2658 | biostudies-arrayexpress
Project description:The homeostasis of circulating B cell subsets in the peripheral blood of healthy adults is well regulated, but in disease it can be severely disturbed. Thus, a subgroup of patients with common variable immunodeficiency (CVID) presents with an extraordinary expansion of an unusual B cell population characterized by the low expression of CD21. Since these circulating atypical B cells in the blood of CVID patients could not be assigned to any certain B cell differentiation stage in the periphery, they were designated as CD21low B cells. Although, CD21low B cells are polyclonal and unmutated IgM+IgD+ B cells like naive B cells in the peripheral blood, they reveal several distinct phenotypic and functional features. In order to uncover the the global programme of gene expression underlying these differences and changes in CD21low B cells we have performed microarray hybridization experiments and identified differentially expressed genes which define a distinct gene expression profile in CD21low B cells compared to naive B cells. Leucocytes were separated by Ficoll gradient from peripheral blood of healthy donors (HD) and CVID patients. CD19+CD27-CD38+CD21+ naive B cells of HD as well as naive and CD19hiCD27-CD38lowCD21low (CD21low) B cells of CVID patients were sorted using a MoFlow cell sorter. RNA was extracted from sorted ex vivo B cell subpopulations and hybridized on Affymetrix microarrays. Gene expression profiles were compared between CD21low B cells and naive B cells of CVID patients as well as HD naive B cells.
2009-07-30 | E-GEOD-17269 | biostudies-arrayexpress
Project description:Variation in individuals' adaptive immune response is believed to influence susceptibility to complex diseases in humans. The genetic basis of such variation is poorly understood. We measured gene expression from resting and activated CD4+ T cells derived from the peripheral blood of healthy individuals. We activated the primary T cells with anti-CD3/CD28 beads alone or with IFNb or Th17 polarizing cytokines. We collected peripheral blood from each human donor. We isolated peripheral blood mononuclear cells by Ficoll, and negatively selected for CD4+ T cells using RosettaSep. We then either left cells unstimulated or stimulated them with beads conjugated with anti-CD3 and anti-CD28 either without additional cytokines, or with IFNb, or with Th17 cocktail. Cells were harvest at up to 8 time points (0hr, 45min, 2hr, 4hr, 10hr, 24hr, 48hr and 72hr), lysed and RNA isolated to be profiled on microarray.
2014-08-28 | E-GEOD-60234 | biostudies-arrayexpress
Project description:Shiga toxin type 2 (Stx2) is the main virulence factor produced by Stx-producing Escherichia coli (STEC) responsible for hemorrhagic colitis and the life-threatening sequela hemolytic uremic syndrome.
2022-11-21 | PXD038256 |
Project description:Analysis of differentiated Caco-2 intestinal epithelial cell line cocultured with probiotics L. acidophilus NCFM™, B. lactis 420, L. salivarius Ls-33 bacterial cells or treated with cell-free supernatant, and with E. coli O157:H7 cell-free supernatant. Lactobacillus and Bifidobacterium are important genera suggested to be beneficial for human health and E. coli O157:H7 is a pathogen causing hemorrhagic colitis and hemolytic uremic syndrome. Results provide insight into the mechanisms underlying the beneficial effects of probiotics on intestinal epithelial cells and a comparison to pathogenic E. coli.
2009-04-11 | GSE15636 | GEO
Project description:CD46 is well known to be involved in diverse biological processes. Although several splice variants of CD46 have been identified, little is known about the contribution of alternative splicing to its tumorigenic functions. Here we found that exclusion of CD46 exon13 is significantly increased in bladder cancer samples. In bladder cancer cell lines, enforced expression of CD46-CYT2 (exon13-skipping isoform) induced cell growth and migration, and promoted tumorigenicity in a xenograft model. While enforced expression of CD46-CYT1 (exon13-containing isoform) attenuated tumorigenicity, representing an inverse phenotype of CD46-CYT2. We also used RNA sequencing to identify changes in gene expression after CD46-CYT1 or CD46-CYT2 overexpression and found KRT19 is a key CD46-CYT2 target gene. Furthermore, we applied interaction proteomics to identify exhaustively the complexes containing CYT1 or CYT2 domain in EJ-1 cells. 320 proteins were identified that interact with CYT1 or/and CYT2 domain, including some well-known CYT1 partners and most of them are new interactors. The new CYT2 partners’ translation machinery, RPL17 and EIF5A, were confirmed by coimmunoprecipitation experiments. We demonstrated that CD46-CYT2 enhances mRNA translation perhaps through an interaction with the translation machinery. Strikingly, the splicing factor SRSF1 is upregulated in bladder cancer and stimulates exclusion of exon13. Importantly, SRSF1 is highly correlated with CD46 exon13 exclusion in clinical bladder cancer samples. Taken together, our findings contribute to understanding the role of CD46 in bladder cancer development.
2019-12-31 | GSE117135 | GEO