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Hippocampal interferon-response, unfolded-protein-response and synaptic transcriptional signatures in RORgt-transgenic mice

ABSTRACT: RORgt-transgenic mice provide a model of sustained Th17 bias. We performed bulk RNA sequencing of bilateral hippocampi from untreated 10-week-old male RORgt-transgenic mice and wild-type littermates (n = 3 per genotype) to characterize gene-level and gene-set transcriptional differences. RNA-seq identified a small set of FDR-significant genes and gene-set enrichment patterns involving interferon responses, unfolded protein response, and synaptic/calcineurin-related processes. The dataset is intended to support transparent reanalysis of the hippocampal transcriptomic phenotype associated with the RORgt-transgenic genotype.

ORGANISM(S): Mus musculus

PROVIDER: GSE347403 | GEO | 2026/09/16

REPOSITORIES: GEO

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Hippocampal interferon-response, unfolded-protein-response and synaptic transcriptional signatures in RORgt-transgenic mice

Project description:Hippocampal interferon-response, unfolded-protein-response and synaptic transcriptional signatures in RORgt-transgenic mice

| PRJNA1529740 | ENA

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

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

2011-06-20 | GSE29777 | GEO

Tfam-Mediated Metabolic Perturbation in RORgt+ Lymphocytes Impacts Intestinal Tissue Homeostasis and Promotes GATA3+RORgt+ Innate Lymphoid Cells

Project description:Rorc-mediated deletion of Tfam, a mitochondrial transcription factor, causes tuft cell-type 2 immunity-driven small intestine (SI) lengthening in mice. Here, we report an indispensable role for Th2 cells in this process. High-fat diet (HFD) reverts SI lengthening in Tfamf/fRorc-cre mice by suppressing IL-13-producing Th2 cells and IL-17-producing Th2 and ILC2s. HFD reduces conventional GATA3–/loRORgt+ ILC3s, but promotes GATA3+RORgt+ ILCs, especially in Tfamf/fRorc-cre mice. Compared to conventional ILC3s, GATA3+RORgt+ ILCs express type 2 cytokines, increase cell proliferation but decrease cell death with metabolic reprograming. Single-cell transcriptional analyses indicate that GATA3+RORgt+ ILCs represent a distinct population, different from IL-17– natural ILC2s, IL-17+ inflammatory ILC2s, or conventional ILC3s. GATA3+RORgt+ ILCs produce IL-17 but not IL-22, resulting from competition of the aryl hydrocarbon receptor (Ahr) with GATA3 at the Il22 locus. Tfamf/fRorc-cre mice on HFD have worsened DSS-induced colitis. These data highlight the role of ILC metabolism in intestinal tissue remodeling and inflammation.

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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

Foxp3+RORgt+ TCR Sequencing

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

| PRJEB15258 | ENA

ATAC-seq of wild type and Stat3-deficient or Rorgt-deficient Th17 cells

Project description:STAT3 has a more profound effect on chromatin accessibility regulation than RORgt during Th17 cell differentiation.

2020-07-30 | GSE153442 | GEO

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

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.

2014-03-07 | GSE53455 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of RNAs bound by DDX5 and RORgt in cultured T helper 17 cell [RIP-seq]

Project description:Purpose: The goals of this study are to compare RNAs bound by DDX5 and RORgt in cultured T helper 17 cell in wildtype background. Methods: Th17 mRNA profiles of 48hrs in vitro cultured T helper 17 cells from wild-type mice were generated by deep sequencing, using Illumina HighSeq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: BurrowsâWheeler Aligner (BWA) and TopHat followed by CuffDiff. qRTâPCR validation was performed using SYBR Green assays. Results: Among the 3444 RefSeq non-coding RNAs and 46449 NONCODE non-coding RNAs, 2533 were found to be expressed in Th17 cells (FPKM>1). 210 of them were enriched in DDX5 pull-down and 119 of them were enriched in RORgt pull-down. Conclusions: Our study suggest that a subset of 31 ncRNAs were co-enriched in DDX5 and RORgt pull-down. DDX5 or RORgt-associated-RNA profiles of 48hr in vitro cultured Th17 from wild type (WT) mice were generated by deep sequencing using Illumina HighSeq

2015-12-21 | E-GEOD-70109 | biostudies-arrayexpress

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