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Expression profiling comparisons of human CD4+ T cells treated with RORgt inhibitors

ABSTRACT: The aim of this study was to identify differential gene expression resulting from the inhibition of RORgt in human CD4+ T cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53455 | GEO | 2014/03/07

SECONDARY ACCESSION(S): PRJNA232048

REPOSITORIES: GEO

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Expression profiling comparisons of human CD4+ T cells treated with RORgt inhibitors

Project description:The aim of this study was to identify differential gene expression resulting from the inhibition of RORgt in human CD4+ T cells. Human CD4+ T cells were cultured with anti-CD3/anti-CD28 mAb for 20 to 60 hours concurrent with exposure to Vehicle (DMSO), TMP778 (0.2 uM) or TMP776 (0.2 uM). All samples were then processed for RNA extraction, labeling, and hybridization to Affymetrix arrays.

2014-03-07 | E-GEOD-53455 | biostudies-arrayexpress

Expression profiling comparisons of human PBMC treated with class I/IIb or class IIa HDAC inhibitors

Project description:The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in human PBMC.

2013-03-24 | GSE44621 | GEO

Gene expression profiling of small intestine (SI) NKp46+RORgt+ and NKp46+RORgt- Innate Lymphoid Cells (ILCs)

2011-06-20 | GSE29777 | GEO

Gene expression profiling of small intestine (SI) NKp46+RORgt+ and NKp46+RORgt- Innate Lymphoid Cells (ILCs)

Project description:The aim of this study was to analyze the global transcriptional profiles of small intestine (SI) Innate Lymphoid Cells (ILCs) expressing the NK cell marker NKp46. Based on differential expression of the RORgt transcription factor SI NKp46+ ILCs can be divided in NKp46+RORgt- and NKp46+RORgt+ cells. While NKp46+RORgt- cells produce IFN-g, like conventional Natural Killer (NK) cells, NKp46+RORgt+ cells secrete IL-22, like Lymphoid Tissue inducer (LTi) cells. We compared the global transcriptional profiles of both NKp46+RORgt- and NKp46+RORgt+ cells to conventional splenic NK cells and to SI NKp46-RORgt+ cells, which contain adult LTi cells. By following this approach, we showed that SI NKp46+RORγt- ILCs correspond to SI NK cells. We also identified a transcriptional program conserved in adult SI NKp46+RORγt+, NKp46-RORγt+ ILCs and fetal LTi. The various ILC cell populations analyzed in this study were isolated from C57BL/6 RORc(gt)+/GFP reporter mice. SI NKp46+RORγt- (NKp46+GFP-) cells, SI NKp46+RORγt+ cells (NKp46+GFPlow and NKp46+GFPhigh cells) and NKp46-RORγt+ ILCs, including adult LTi cells , were sorted by flow cytometry from CD3- lamina propria cells of small intestine (SI) of RORc(γt)+/GFP reporter mice . Splenic NKp46+RORγt- (NKp46+GFP-) cells were also sorted as the reference for conventional NK cells. Two replicates of each populations were produced and analyzed.

2011-06-20 | E-GEOD-29777 | biostudies-arrayexpress

Expression profiling comparisons of human PBMC treated with class I/IIb or class IIa HDAC inhibitors

Project description:The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in human PBMC. Human PBMC were cultured ex vivo with a mitogenic stimulus (1 ug/ml phytohemagglutinin, PHA) for 60 hours concurrent with exposure to vehicle (DMSO), vorinostat (3 uM), or TMP195 (3 uM). In addition to the whole PBMC populations, a portion of the cultures treated with DMSO or TMP195 were used for FACS purification of mutually exclusive CD3+ (T cell), CD19+ (B cell), and CD14+ (monocyte) populations. All samples were then processed for RNA extraction, labeling, and hybridization to Affymetrix arrays. Vehicle vs. vorinostat vs. TMP195 treatments in PBMC; Vehicle vs. TMP195 treatment in CD3+, CD19+ or CD14+ cells

2013-03-24 | E-GEOD-44621 | biostudies-arrayexpress

Gene expression profile at single cell level of tissue- associated kidney NKp46+NK1.1+ or NK1.1+ ILC from untreated and poly (I:C) treated RORgt-FM mice

Project description:We next asked whether RORgt-FM+ ILC are transcriptionally similar to the Tnfrsf9+ tILC that we identified in lupus-prone mice. To explore this, we isolated tissue RORgt-FM+ and RORgt-FM- NKp46+ ILC from RORgt-FM mice, some of which were treated with poly(I:C) and analyzed them by scRNA-seq

2024-07-11 | GSE269400 | GEO

Decoupling the role of RORgt in the differentiation and effector function of Th17 cells

Project description:RORgt is known to instruct the differentiation of Th17 cells that mediate the pathogenesis of autoimmune diseases. However, it remains unknown whether RORgt plays a distinct role in the differentiation and effector function of Th17 cells. Here we show that mutation of RORgt lysine 256, a ubiquitination site, to arginine (K256R) separates the RORgt role in these two functions. Preventing ubiquitination at K256 via arginine substitution does not affect RORgt-dependent thymocyte development and Th17 differentiation in vitro and in vivo, however, greatly impaired the pathogenesis of Th17 cell-mediated experimental autoimmune encephalomyelitis (EAE). Mechanistically, K256R mutation impairs RORgt to bind to and activate Runx1 expression critical for Th17-mediated EAE. Thus, RORgt regulates the effector function of Th17 cells in addition to Th17 differentiation. This work informs the development of RORgt-based therapies that specifically target the effector function of Th17 cells responsible for autoimmunity.

2022-10-26 | GSE211509 | GEO

Microarray expression profiling of MAIT subsets isolated from thymus of B6-MAIT/CAST mice, as compared to single positive CD4 or CD8 conventional T cells.

Project description:In mice, contrary to conventional T cells, MAIT cells acquire a memory phenotype in the thymus in relation with Zbtb16 expression (Savage et al., 2008 ; Koay et al., 2016). To define phenotypic transcriptional signatures of MAIT subsets in the thymus, we analyzed by microarray the transcriptome of MAIT1 (MR1tet+RORgt+) and MAIT17 (MR1tet+RORgt+) as compared to conventional mature (TCRb+CD24lo) CD4+ and CD8+ single positive cells.

2019-07-01 | E-MTAB-7702 | biostudies-arrayexpress

Foxp3+RORgt+ TCR Sequencing

Project description:TCR repertoire sequencing of mucosal Foxp3+RORgt+ regulatory T cells

| PRJEB15258 | ENA

Effect of DDX3 inhibitors on CD4+ T cells

Project description:An innovative approach to eliminate HIV-1-infected cells emerging out of latency, the major hurdle to HIV-1 cure, is to pharmacologically reactivate viral expression and concomitantly trigger intracellular pro-apoptotic pathways in order to selectively induce cell death (ICD) of infected cells, without reliance on the extracellular immune system. In this work we demonstrate the effect of DEAD-box polypeptide 3, X-Linked (DDX3) inhibitors on selectively inducing cell death in latent HIV-1-infected cell lines, primary CD4+ T cells and in CD4+ T cells from cART-suppressed people living with HIV-1 (PLWHIV). RNA sequencing analysis revealed that while overall gene expression was minimally dysregulated, DDX3 inhibition in independent donor CD4+ T cells led to significant downregulation of BIRC5 and HSPB1A, genes critical to cell survival during HIV-1 infection. We used single-cell FISH-Flow technology to characterise latency reversal and the contribution of viral RNA to inducing cell death; pharmacological targeting of DDX3 induced HIV-1 RNA expression, resulting in phosphorylation of IRF3, upregulation of IFNβ and selective induction of apoptosis in viral RNA-expressing CD4+ T cells from PLWHIV but not bystander cells. DDX3 inhibitor treatment of CD4+ T cells from PLWHIV in an in vitro culture model over five days resulted in an approximately 50% reduction of the inducible latent HIV-1 reservoir as determined by quantitation of CA HIV-1 RNA, by TILDA, as well as by FISH-Flow technology. Our data support the translation of DDX3 inhibitor class compounds into HIV-1 curative strategies and provide proof of concept for pharmacological reversal of latency coupled to induction of apoptosis towards elimination of the inducible reservoir.

2021-02-26 | GSE167553 | GEO

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