Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA112557 | ENA |
REPOSITORIES: ENA
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Project description:Parental and BXD mouse lines were received from Jackson Laboratory and The Oak Ridge National Laboratory. Splenocytes were isolated and stained with anti-CD4 and anti-CD25 antibodies. CD4+ T cells were separated into CD4+CD25+ Treg and CD4+CD25- Th cells. Tregs and Th cell were collected from spleens of 31 BXD recombinant inbred strains and of the parental mouse strains DBA/2J and C57BL/6J. Gene expression was measured by microarrays. The comparative analysis of the transcriptomes from the two cell populations allowed us to identify many novel differentially expressed genes. Furthermore, the analysis of cis- and trans-expression Quantitative Trail Loci (eQTLs) showed that both common and unique regulatory mechanisms are active in the two cell types.
2011-12-15 | E-MTAB-836 | biostudies-arrayexpress
Project description:Goals and objectives of this study: to identify genes of the Treg signature induced by consitutive expression of GARP or FOXP3 in antigen-specific Th cells with potential role for stabililization & maintenance of the regulatory program. Keywords: T-cell receptor stimulation, gene-regulation, comparative gene expression profiling, cell type comparison, human, regulatory T cells, FOXP3, GARP Human alloantigen-specific Treg cells (THU) and Th cells (CD4-39), established and described recently (Ocklenburg et al.. Lab Invest.2006; 86: 724-737), were sitmulated for 3 days with cognate antigen (EBV B cells) and IL2 as described (Ocklenburg et al.. Lab Invest.2006; 86: 724-737) and analyzed using human Affymetrix U133 2.0 in monoplicate. Th cells had been transduced with a retroviral vector containing human GARP (LRRC32) or FOXP3 and an IRES-driven GFP as marker or empty GFP control, sorted for GFP+, expanded as described recently (Ocklenburg et al.. Lab Invest.2006; 86: 724-737), and characterized functially, phenotypically, and genetically as described (WO/2007/113301). Abbreviations: Treg THU d3 = alloantigen-specific Treg cells; GFP d3 = GFP-transduced alloantigen-specific Th cells (CD4-39); FoxP3 d3 = FOXP-transduced alloantigen-specific Th cells (CD4-39); Garp d3 = GARP-transduced alloantigen-specific Th cells (CD4-39); all stimulated for 3 days (=d3) with EBV B cells and IL2.
2009-04-20 | E-GEOD-13234 | biostudies-arrayexpress
Project description:Transcriptome analysis of freshly sorted regulatory T cells (CD4+CD25+) and conventional T cells (CD4+CD25-) and of expansion cultures of regulatory T cells (CD4+CD25+CD45RA+) and conventional T cells (CD4+CD25-). Three biological replicates were performed of freshly sorted Treg and Tconv cells each. Four replicates of Treg expansion cultures sorted into CD45RA+/- subpopulations prior to RNA extraction were performed.
2009-05-20 | E-GEOD-14232 | biostudies-arrayexpress
Project description:A microarray study was performed in unstimulated and TCR-stimulated CD4 + T cells and Treg in wild type and conditional Trim28 KO mice to identify genes that are regulated by Trim28. These experiments constitute a portion of the study described below: Paper Abstract: Peripheral T cell activation and differentiation into specialized effectors are regulated by TCR- and cytokine-mediated signals that induce clonal expansion and unique transcriptional factors. These processes may include active chromatin modification by nuclear factors. In search of such molecules, we found Trim28, a component of large nuclear chromatin-regulatory complex is tightly controlled upon TCR stimulation at the level of phosphorylation, and examined global impact of Trim28 loss in especially CD4+ T cells, by generating T cell-specific conditional Trim28 KO mice (CKO). CD4+ T cells from CKO mice showed defective IL-2 production and T cell proliferation associated with defective upregulation of cell-cycle associated proteins. Accordingly, young CKO showed T-lymphopenia. Surprisingly, Trim28 CKO mice eventually accumulated auto-reactive memory-phenotype T cells that produced inflammatory IL-17. CKO mice are also susceptible to induced auto-inflammatory disease with TH-17 dominant immune response. Loss of Trim28 showed aberrant accumulation of TH-17 and FoxP3+ T cells, two key T cells in inflammation vs. tolerance. We found CKO T cells showed a cell-extrinsic promotion of TH-17 and FoxP3+ T cell development by a mechanism involving overproduction of TGF-beta. Our study revealed unexpected roles of Trim28, a global chromatin regulator in both T cell activation and tolerance. Trim28 conditional KO mice and age-matched control mice were sacrificed, and neive CD4+ T cells (CD4+CD62+CD25-) and Treg (CD4+CD62+CD25+) were sorted. Stimulation of naive T cells was done with anti-CD3 and anti-CD28 for 13 hours. We collected quadruplicates for each group.
2012-04-28 | E-GEOD-32224 | biostudies-arrayexpress
Project description:The immune system faces a task that approximates cognition in its complexity as it processes a multitude of intrinsic and extrinsic signals and integrates these into responses of the appropriate class, specificity, magnitude, and duration for a given threat, with the host’s life often depending on the outcome. CD4+ T lymphocytes occupy a unique role in the generation and regulation of immunity within this context and influence multiple innate and adaptive cell types. With respect to CD8+ cytotoxic T lymphocytes (CTL), CD4+ T cells function early in the response as ‘helpers’ (TH) to increase its magnitude and functionality, and later as regulatory cells (Treg) to restore homeostasis and avoid immune pathology. Using a Listeria monocytogenes (Lm) infection model, we probed whether the conditions of initial pathogen encounter could influence the generation of TH versus Treg. Infection induces rapid polyclonal conversion to functional FoxP3+CD25+ Treg within 24 hours. These findings resolve long-standing questions regarding the requirement for TH and reveal a remarkable degree of plasticity in the function of CD4+ T cells, which can be quickly converted to Treg in vivo in response to acute inflammation.
2021-03-27 | GSE169741 | GEO
Project description:Regulatory T cells (Tregs) suppress other immune cells and are indispensable for human health, yet the molecular mechanisms of suppression remain incompletely understood. Tregs can suppress proliferation and cytokine production of CD4+CD25- conventional T cells (Tcons). We previously demonstrated that human Tregs rapidly suppress T cell receptor (TCR)-induced calcium, NFAT and NF-κB pathways in Tcons, leading to inhibition of effector cytokine transcription (Schmidt A et al., Science Signaling 2011 Dec 20;4(204):ra90. doi: 10.1126/scisignal.2002179). Due to the short time period required to induce suppression, it is probable that Tregs alter protein modifications, such as (de)phosphorylations, in suppressed Tcons to cause this inhibition of particular TCR signaling events, while de novo production of repressor proteins seems unlikely. Thus, in order to identify causative factors which initiate rapid Treg-mediated suppression of Tcons, we compared phosphoproteomes of 5 minutes TCR-stimulated responder Tcons re-isolated from cocultures with primary human Tregs with those from control cocultures (Tcons cocultured with other Tcons). In addition, we measured the basal state of the phosphoproteome in unstimulated Tcon of the same donors. In total, we provide phosphoproteomics data of primary human CD4+CD25- T cells from three human healthy donors each for (i) unstimulated Tcons, (ii) 5 minutes TCR-stimulated Tcons, (iii) 5 minutes TCR-stimulated and Treg-suppressed Tcons.
2017-08-28 | PXD004291 | Pride
Project description:CD4+CD25+FOXP3+ human regulatory T cells (Treg) are essential for self-tolerance and immune homeostasis. Here, we generated genome-wide maps of poised and active enhancer elements marked by histone H3 lysine 4 monomethylation and histone H3 lysine 27 acetylation for CD4+CD25highCD45RA+ naive and CD4+CD25highCD45RA- memory Treg and their CD25- conventional T cell (Tconv) counterparts after in vitro expansion . In addition we generated genome-wide maps of the transcription factors STAT5, FOXP3, RUNX1 and ETS1 in expanded CD4+CD25highCD45RA+ Treg- and CD4+CD25- Tconv to elucidate their role in cell type-specific gene regulation. ChIP-seq of 2 histone marks and transcription factors ETS1, STAT5, FOXP3 and RUNX1 in expanded T cell subpopulations
2014-04-01 | E-GEOD-43119 | biostudies-arrayexpress
Project description:Functionally distinct CD4+ helper T (Th) cell subsets, such as Th1, Th2, Th17, and regulatory T cells (Treg), play a pivotal role in the host-defense against pathogen invasion and the pathogenesis of inflammatory disorders. In this project, DIA-MS-based proteome analysis was performed on naïve CD4+ T, Th0, Th1, Th2, Th17 and iTreg cells using Q Exactive HF-X (Thermo Fisher Scientific) to search for proteins that differ among the cell subsets.
2023-01-04 | PXD036065 | JPOST Repository
Project description:The immune system faces a task that approximates cognition in its complexity as it processes a multitude of intrinsic and extrinsic signals and integrates these into responses of the appropriate class, specificity, magnitude, and duration for a given threat, with the host’s life often depending on the outcome. CD4+ T lymphocytes occupy a unique role in the generation and regulation of immunity within this context and influence multiple innate and adaptive cell types. With respect to CD8+ cytotoxic T lymphocytes (CTL), CD4+ T cells function early in the response as ‘helpers’ (TH) to increase its magnitude and functionality, and later as regulatory cells (Treg) to restore homeostasis and avoid immune pathology. Using a Listeria monocytogenes (Lm) infection model, we probed whether the conditions of initial pathogen encounter could influence the generation of TH versus Treg. At low dose infection, CD4+ T cells ‘help’ CTLs via CD40-CD40L signaling, while high dose infection induces rapid polyclonal conversion to functional FoxP3+CD25+ Treg within 24 hours. These findings resolve long-standing questions regarding the requirement for TH and reveal a remarkable degree of plasticity in the function of CD4+ T cells, which can be quickly converted to Treg in vivo in response to acute inflammation.
2020-04-20 | GSE106554 | GEO
Project description:Changes in Treg function are difficult to quantify due to the lack of Treg-exclusive markers in humans and the complexity of functional experiments. We sorted naive and memory human Tregs and conventional T cells, and identified genes that identify human Tregs regardless of their state of activation. We developed this Treg signature using Affymetrix human genome U133A 2.0 microarrays. To generate Tregs and Tconvs in multiple states of activation, naïve (CD4+CD25hiCD45RA+) and memory (CD4+CD25hiCD45RA-) Tregs, and naïve (CD4+CD25-CD45RA+) and memory (CD4+CD25-CD45RA-) Tconvs were sorted from blood of 7 healthy adults and RNA was isolated ex vivo or after stimulation for 40h, promoting activation-induced FOXP3 in Tconvs. The gene-expression profile of the eight cell subsets was analyzed. 7 adult healthy control samples were sorted into 4 subsets: naïve (CD4+CD25hiCD45RA+) and memory (CD4+CD25hiCD45RA-) Tregs, and naïve (CD4+CD25-CD45RA+) and memory (CD4+CD25-CD45RA-) Tconvs. These were used for RNA ex vivo and after 40h stimulation with anti-CD3/CD28 beads to induce an activation phenotype.
2016-01-19 | E-GEOD-76598 | biostudies-arrayexpress