Transcriptomic analysis of TCF-7 cKO CD8 T cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA838947 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19241926_1.fastq.gz | Fastqsanger.gz | |||
| SRR19241926_2.fastq.gz | Fastqsanger.gz | |||
| SRR19241927_1.fastq.gz | Fastqsanger.gz | |||
| SRR19241927_2.fastq.gz | Fastqsanger.gz | |||
| SRR19241928_1.fastq.gz | Fastqsanger.gz |
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Project description:T Cell Factor-1, encoded by TCF-7, is a transcription factor that plays an essential role during T cell development and differentiation. In this manuscript we utilized a pre-clinical model provided evidence that TCF-7 is dispensable for the anti-tumor response, and that TCF-7 suppresses key transcriptional factors Eomes and T-bet and molecules responsible for peripheral CD8 T cell cytolytic function. We discovered that TCF-7 regulates NKG2D expression on naïve and activated mouse CD8 T cells, and that peripheral CD8 T cells from TCF-7 cKO utilize NKG2D to clear tumor cells. We also provide evidence that TCF-7 regulates key signaling molecules, including LCK, LAT, ITK, PLC-y1, P65, ERKI/II, and JAK/STATs required for peripheral CD8 T cell persistent function. Our data transcriptomic and protein data uncovered the mechanism of how TCF-7 impacting peripheral CD8 T cell inflammatory cytokine production, CD8 T cell activation, and apoptosis. Our pre-clinical model showed that CD8 T cells from TCF-7 cKO mice did not cause GVHD, but effectively cleared primary tumor cells.
2022-06-30 | GSE203167 | GEO
Project description:Transcriptomic analysis of TCF-7 cKO CD4 T cells
| PRJNA842069 | ENA
Project description:The transcription factor T Cell Factor-1 encoded by (TCF-7) is critical for T cell development. However, the role of TCF-7 on peripheral CD4 T cells mediated allo-immunity was not known. In this report using a clinically relevant model we presented novel finding of how TCF-7 regulates CD4 T cells functions, including CD4 T cells activation, proliferation, differentiation and impacts effector and central memory formation. We uncovered how TCF-7 regulates chemokine receptor which are essential for CD4 T cells migration to the site of inflammation. Our data uncovered how TCF-7 plays critical role in CD4 T cells survival, apoptosis. Using in vivo allo-immunity models and in-vitro studies we demonstrated how TCF-7 plays central role in CD4 T cells mediated damaged to organs like liver, skin and small intestine. We provided both molecular and biochemical and transcriptomic evidence how TCF-7 functionally regulates CD4 T cells mediated apoptosis and cell death, T cell mediated processes, pro-inflammatory and anti-inflammatory cytokines productions in both basal level and after allo-activation. These findings novel findings represent a stem forward to designing target specific approach for CD4 T cells mediated diseases while understand molecular mechanism the role of CD4 T cells in allo-immunity.
2022-07-30 | GSE204747 | GEO
Project description:TCF-1 is an HMG family transcription factor which is known to be activated by the canonical Wnt signaling pathway and modulated by other signals such as those derived from T cell receptor. We found that during CD8 T cell responses, TCF-1 deficiency impaired long-term maintenance of antigen-specific memory CD8 T cells. We used microarrays to detect gene expression changes in memory CD8 T cells caused by TCF-1 deficiency. Host mice that received WT or TCF-1-deficient OT-I CD8 T cells were infected with attenuated Listeria monocytogenes expressing Ova peptide. In memory phase (i.e., more than 80 days post infection), antigen-specific T cells were ioslated by cell sorting. RNA was extracted and hybridized to GeneChip Mouse GENE 1.0 ST arrays (Affymetrix).
2010-10-04 | E-GEOD-20754 | biostudies-arrayexpress
Project description:TCF-1 is an HMG family transcription factor which is known to be activated by the canonical Wnt signaling pathway and modulated by other signals such as those derived from T cell receptor. We found that during CD8 T cell responses, TCF-1 deficiency impaired long-term maintenance of antigen-specific memory CD8 T cells. We used microarrays to detect gene expression changes in memory CD8 T cells caused by TCF-1 deficiency.
2010-10-04 | GSE20754 | GEO
Project description:CD8+ T cell differentiation traditionally results in the emergence of two subsets, Tc1 cells that produce interferon (IFN)-gamma and memory cells that mediate immune protection against pathogen infections. More recently, it has emerged that other specialized CD8+ T cell populations develop in immune responses and are critical to orchestrate complete immune protection. These subsets include tissue-resident memory (Trm) T cells, follicular cytotoxic T cells and two CD8+ T cell subsets that produce interleukin (IL)-17, namely, mucosal-associated invariant T (MAIT) cells and Tc17 cells. Here we investigated the role of TCF-1 in CD8+ T cell differentiation by using Assay for Transposase-Accessible Chromatin sequencing (ATAC-Seq) to determine the chromatin accessibility landscape of CD8+ T cells and how this is controlled by TCF-1. Loss of TCF-1 was associated with global changes in the chromatin architecture in CD8+ T cells leading to increased accessibility of Rorc and Tc17 effector genes IL-17a and IL-17f in Tc17 cells. In contrast, we observed reduced accessibility of Tbx21, Eomes and Irf4 loci in Tc17 cells, genes normally required for the induction of Tc1 and memory CD8+ T cells
2019-05-14 | GSE119839 | GEO
Project description:TCF-1 regulation of CD8+ T cell chromatin accessibility
| PRJNA490437 | ENA
Project description:The present investigation was to identify transcriptomic changes of control and Dnd1-cKO PGCs at E11.5 by RNA-seq analysis. We identified 181 upregulated and 141 downregulated genes in Dnd1-cKO PGCs.
2022-12-28 | GSE218770 | GEO
Project description:Sorted single CD8+T cells expressing CD14 from human liver for SMARTSeq2.
Livers processed: Kucykowicz et al STAR Prot 2022:pubmed.ncbi.nlm.nih.gov/35516846/
Published: Pallett et al Nature 2022
Tissue CD14+CD8+T-cells are reprogrammed by myeloid cells and modulated by LPS
The liver is bathed in bacterial products including LPS transported from the intestinal portal vasculature, but maintains a state of tolerance exploited by persistent pathogens and tumours1,2,3,4. The cellular basis mediating this tolerance, yet allowing a switch to immunity or immunopathology, needs to be better understood for successful immunotherapy of liver diseases. Here we show that a variable proportion of CD8+T-cells compartmentalised in the human liver co-stain for CD14 and other prototypic myeloid membrane proteins; CD14+CD8+T-cells preferentially accumulate within the donor pool in liver allografts, amongst hepatic virus-specific and tumour-infiltrating responses, and in cirrhotic ascites. CD14+CD8+T-cells exhibit increased turnover, activation and constitutive immunomodulatory features with high homeostatic IL-10/IL-2 production directly ex vivo, and an enhanced capacity to rapidly produce antiviral/anti-tumour cytokines upon TCR engagement. This CD14+CD8+T-cell profile can be recapitulated by acquisition of membrane proteins, including the LPS receptor complex, from mononuclear phagocytes, resulting in augmented tumour killing by TCR-redirected T-cells in vitro. CD14+CD8+T-cells express integrins and chemokine receptors favouring interactions with the local stroma, which can promote their induction through CXCL12. LPS can also increase the frequency of CD14+CD8+T-cells in vitro and in vivo, and skew their function towards the production of chemotactic and regenerative cytokines. Thus, bacterial products in the gut-liver axis and tissue stromal factors can tune liver immunity by driving myeloid instruction of CD8+T-cells with immunomodulatory capacity.
For the analysis of the single cell transcriptome two intrahepatic perfusate samples were isolated and frozen at -80 'C for storage prior to transportation to Newcastle, UK. Once thawed in pre-warmed HBSS containing 0.001% DNaseI, intrahepatic leukocytes were sorted by FACS to index classical mononuclear phagocytes (MNP) defined as Singlets, CD3-CD56-CD19-CD14hiHLA-DR+ or CD14± CD8+T-cells as follows: Singlets, CD3+CD56-CD19-CD4-CD8+Vï¡7.2- and split in to CD14± based on an isotype control. Single cells were sorted into 96-well skirted LoBind plates (Eppendorf) containing 5 µL lysis buffer (TCL buffer [Qiagen], supplemented with 1% b-mercaptoethanol [Sigma Aldrich; Merck]) on a BD Bioscience FACSFusion. The sorted plates were subsequently immediately sealed, centrifuged, and placed on dry ice to flash-freeze the cell lysate and stored at -80 'C.
A modified SMART-seq2 protocol57 was performed on the single flow cytometry sorted-cells as previously described58. After cDNA generation, libraries were prepared (384 cells per library) using the Illumina Nextera XT kit (Illumina). Each library was sequenced to achieve a minimum depth of 1-2 million raw reads per cell using an Illumina HiSeq 4000 using v. 4 SBS chemistry to generate 75-bp paired-end reads.
| EGAS00001006885 | EGA
Project description:The present investigation was to identify transcriptomic changes of control and Dnd1-cKO PGCs at E12.5 and E13.5 by microarray comparison. We identified 1470 upregulated and 924 downregulated genes in Dnd1-cKO PGCs.
2022-12-28 | GSE218744 | GEO