MRNA profiling of human effector Type 1 T helper (Th1) cells for autoimmune gene signatures using the nCounter Nanostring platform [autoimmunity panel]
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE298667 | GEO | 2025/12/31
REPOSITORIES: GEO
Similar Datasets
Project description:Human naïve CD4 T cells were purified from healthy volunteers' peripheral blood using commercially available kits and differentiated into effector Th1 in vitro by culturing for 6 days in the presence of anti-CD3 and CD28 antibodies (2 µg/ml each) and IL-12 (20 ng/ml). Human effector Th1 cells were harvested on day 6 post-differentiation and treated with either vehicle, LY (0.0125 µM), or Methyl Pyruvate (MePyr, 5 mM) in complete RPMI media for 24 hours.
2025-12-31 | GSE298668 | GEO
Project description:CD4 T cells were activated using CD3/CD28 antibodies in the presence of IL2 and IL12, to generate Th1 cells. Th1 cells were maintained and expanded in IL2 and IL12, on D5 Th1 cells were sorted for CD4+ expression and DAP1 exclusion. After flow sorting, live TH1 cells were resuspended (1e6 per ml) in methionine free RPMI, supplemented with 10% dialysed FBS, IL2 and IL12, and with L-methionine (100μM, or 1μM). Cells were cultured for 5 hrs before collection for proteomics processing.
2019-03-29 | PXD012053 | Pride
Project description:Gene expression profiling of repeatedly activated compared to recently activated Th1 cells to identify genes that play a role in chronic inflammatory disorders and may qualify as diagnostic or therapeutic targets; ; Upon activation under appropriate costimulatory conditions, naive T helper (Th) cells differentiate into Th2 or Th17 cells, each characterized by the expression of specific effector cytokines. In response to a repeated stimulation with antigen, Th cells develop a stable memory for the expression of those cytokines as well as for other secreted or membrane-associated factors. The stable memory for the expression of proinflammatory effector functions may explain the resistance of Th effector cells to conventional immunosuppressive therapy, and the inability of immunosuppression to cure chronic inflammation. The imprinting of the functional memory is based on epigenetic modifications and expression of distinct transcription factors. In this project, we compare the transcriptomes of once and repeatedly activated murine Th1 cells, to identify genes that induce and maintain the functional memory and control the persistence of pathogenic memory Th1 cells. This in turn might help to discriminate pathogenic versus protective cells in immunopathology and present novel targets for the diagnosis and therapy of chronic inflammatory disease. Experiment Overall Design: Genes differentially expressed in once versus four times stimulated Th1 cells. In vitro polarization of murine naïve DO11.10 T cells towards Th1 direction (5 ng/ml recombinant murine IL-12, 5 μg/ml anti-IL-4 antibody) with antigenic stimulation (ova323-339 and irradiated splenic APCs). The transcriptional profiles of resting one week old Th1 (Th1 1w) cells and resting 4 week old Th1 (Th1 4w) cells were compared using Affymetrix Murine Genome (MG) U74V2A GeneChip arrays. Experiment Overall Design: 10 µg of total RNA from each cell sample was reverse transcribed using T7-(d)T24 primer and SuperScript II reverse transcriptase Experiment Overall Design: cDNA extraction with a PhaseLock gel (Eppendorf), and precipitation with ethanol and ammonium acetate Experiment Overall Design: Biotinylated cRNA was transcribed with the MEGAscript high yield transcription kit (Ambion), fragmented, and the hybridization cocktail was prepared (15 µg fragmented biotin-labeled cRNA spiked with Eukaryotic Hybridization control) Experiment Overall Design: probes were subsequently hybridised with the GeneChip U74Av2 for 16 hrs at 45 oC Experiment Overall Design: after washing the hybridisation signals were visualised by staining with streptavidin-phycoerythrin and amplification with an anti-streptavidin antibody Experiment Overall Design: TH1_1w_C1; TH1_1w_C2; TH1_1w_C3TH1_4w_C1; TH1_4w_C2; TH1_4w_C3 Experiment Overall Design: 1w: 1 week in culture; 4w: 4 weeks in culture; C1-3: Culture or Experiment No.
2008-06-18 | E-GEOD-11534 | biostudies-arrayexpress
Project description:We report the differential mRNA expressino of WT and Chi3l1 KO Th1 cells. We cultured WT and Chi3l1 KO naive CD4 T cells under Th1 skewing condition : plate-bound anti-CD3/28 antibody (2ug/mL), IL-12 0.2ng/mL, IL-2 50U/mL, anti-IL-4 neutralizing antibody 2ug/mL, for 3 days. We found different Th1 regulatory and tumoricidal-related gene expression in Chi3l1 KO T cells.
2018-02-13 | GSE105056 | GEO
Project description:Naïve CD4+ T cells were isolated from spleen of AND TcR transgenic/green fluorescence protein (GFP) transgenic mice (Kaye et al., Nature 1989;341:746, Wright et al, Blood 2001;97:2278) that recognize a peptide of pigeon cytochrome C in the context of I-Ek and express CD44lo, CD62Lhi, CD45RBhi, and CD25-. After 4 days in vitro stimulation with antigen presenting cells (APC) under either Th1 or Th2 condition, naïve cells become Th1 or Th2 effector cells expressing CD44hi, CD62L lo, CD45RBhi, and CD25+. Additional 3 days culture in the absence of APC, those effector cells become rested expressing a phenotype similar to memory cells (CD44 hi, CD62L lo, CD45RB lo and CD25-). These rested effector cells were adaptively transferred into thymectomized, lethally irradiated, and T cell depleted bone marrow reconstituted mice and memory cells were isolated after 4-12 weeks by flow sort. Generation and purification of Th1 and Th2 effector and memory CD4+ T cells of 42 samples.
2010-06-10 | E-GEOD-8352 | biostudies-arrayexpress
Project description:Th17 cells have better stemness and differentiation potential, and under certain circumstances, they can be stimulated to differentiate into other subcelltypes including Th1 and Treg. Here, we report that compared to traditional Th1 and Th17 cells, Th17-derived Th1 cells had greater anti-tumor activity. Both C57 mice ACT therapy and CAR-T therapy models were used to validate it. Mechanism: Th17-derived Th1 cells are able to express Th1 effector molecules as well as retain a lower level of exhaustion than Th1 cells. Additionally, it has a higher amount of type 1 interferon response and a stronger capacity for migration. Our research offers a fresh perspective on how ACT therapy and CAR-T therapy might develop in the future.
2024-10-31 | GSE276409 | GEO
Project description:There is evidence that microglia interact with infiltrating Th1 and Th17 cells and this interaction results in mutual activation. However, the potential of a distinct cytokine milieu generated by these effector T cell subsets to activate microglia is poorly understood. In this study, we tested the ability of factors secreted by Th1 and Th17 cells to induce microglial activation. Interestingly, we found that only Th1-associated factors had the potential to activate microglia while the Th17-associated factors as well as direct contact of Th17 cells with microglia only had a minimal effect. Further Th1-derived factors triggered a proinflammatory M1-type gene expression profile in microglia Microglia harvested from mixed glial cultures were treated with supernatants from Th1- or Th17 cultures. Microglia cultured in medium was used as controls. At 16h post treatment RNA was isolated from the microglia and probed on Agilent´s murine 4x44k microarrays. RNA isolated from four independent experiments were used for the gene expression profiling. Microglia, Th1, Th17
2013-12-31 | E-GEOD-45384 | biostudies-arrayexpress
Project description:We aimed to gain a comprehensive understanding of transcriptional profiles of circulating Th1, Th1/17, and Th17 cells in endometriosis patients (n=10) as compared to healthy controls (n=12). Briefly, fresh peripheral blood was collected from subjects, peripheral blood mononuclear cells (PBMCs) were isolated using density centrifugation and then cryopreserved until later bulk analysis. PBMCs were later thawed, CD4+ T cells were magnetically isolated (#17952, StemCell Technologies, Canada) and stimulated with 30ng/mL of PMA and 1ug/mL of Ionomycin and incubated for 4hrs. Cells were then stained for FACS and sorted into viable populations of Th17 (CD3+CD4+IFNg-IL-17+), Th1/17 (CD3+CD4+IFNg+IL-17+), and Th1 (CD3+CD4+IFNg+IL-17-) cells using BD FACSAria™ III. RNA was then isolated from Th1, Th1/17, and Th17 cell populations from patients and controls using a commercially available kit (#74004, Qiagen, Canada). Samples were then quality checked and sent for bulk RNA sequencing (RNAseq) at McGill Genome Centre (MGC, Canada) using Illumina NovaSeq X Plus 10B (Illumina, USA) and subsequent bioinformatic analyses, as per standard pipelines. Briefly, analyses included principal component analysis (PCA), unsupervised and supervised clustering, heatmap generation, differential expression analysis (DEG), volcano plots, fold-change distribution, and Gene Ontology (GO) enrichment analyses. RNA sequencing revealed extensive Th subset reprogramming in endometriosis, most predominately in Th17 cells (2,220 DEGs). Collectively, our findings reveal significant immune remodeling in endometriosis and highlight a distinct, aberrant Th17 cell phenotype, contributing to endometriosis pathophysiology. Ultimately, this work supports the repurposing of IL-23- and IL-17-targeted therapeutics to provide novel options for endometriosis patients, as these therapeutics have been successfully used in other chronic inflammatory diseases and may also target endometriosis-associated comorbidities.
2025-12-15 | GSE313775 | GEO
Project description:Memory helper T (Th) cells are crucial for secondary immune responses against infectious microorganisms but also drive the pathogenesis of chronic inflammatory diseases. Therefore, it is of fundamental importance to understand how memory T cells are generated. However, the molecular mechanisms governing memory Th cell generation remain incompletely understood. Here, we identified CD30 as a molecule heterogeneously expressed on effector Th1 and Th17 cells, and CD30hi effector Th1 and Th17 cells preferentially generated memory Th1 and Th17 cells. We found that CD30 mediated signal induced Transglutaminase-2 (TG2) expression, and that the TG2 expression in effector Th cells is essential for memory Th cell generation. In fact, Cd30-deficiency resulted in the impaired generation of memory Th1 and Th17 cells, which can be rescued by overexpression of TG2. Furthermore, transglutaminase-2 (Tgm2)-deficient CD4 T cells failed to become memory Th cells. As a result, T cells from Tgm2-deficient mice displayed impaired antigen-specific antibody production and attenuated Th17-mediated allergic responses. Our data indicate that CD30-induced TG2 expression in effector Th cells is essential for the generation of memory Th1 and Th17 cells, and that CD30 can be a marker for precursors of memory Th1 and Th17 cells.
2020-06-04 | GSE151691 | GEO
Project description:Memory helper T (Th) cells are crucial for secondary immune responses against infectious microorganisms but also drive the pathogenesis of chronic inflammatory diseases. Therefore, it is of fundamental importance to understand how memory T cells are generated. However, the molecular mechanisms governing memory Th cell generation remain incompletely understood. Here, we identified CD30 as a molecule heterogeneously expressed on effector Th1 and Th17 cells, and CD30hi effector Th1 and Th17 cells preferentially generated memory Th1 and Th17 cells. We found that CD30 mediated signal induced Transglutaminase-2 (TG2) expression, and that the TG2 expression in effector Th cells is essential for memory Th cell generation. In fact, Cd30-deficiency resulted in the impaired generation of memory Th1 and Th17 cells, which can be rescued by overexpression of TG2. Furthermore, transglutaminase-2 (Tgm2)-deficient CD4 T cells failed to become memory Th cells. As a result, T cells from Tgm2-deficient mice displayed impaired antigen-specific antibody production and attenuated Th17-mediated allergic responses. Our data indicate that CD30-induced TG2 expression in effector Th cells is essential for the generation of memory Th1 and Th17 cells, and that CD30 can be a marker for precursors of memory Th1 and Th17 cells.
2020-05-28 | GSE151301 | GEO