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Transcriptional profile of Smad4-deficient CTLs is similar to TRM

ABSTRACT: Transcriptional profile of Smad4-deficient CTLs is similar to TRM

PROVIDER: PRJNA636744 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11907302_1.fastq.gz	Fastqsanger.gz
	SRR11907302_2.fastq.gz	Fastqsanger.gz
	SRR11907303_1.fastq.gz	Fastqsanger.gz
	SRR11907303_2.fastq.gz	Fastqsanger.gz
	SRR11907304_1.fastq.gz	Fastqsanger.gz

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Transcriptional profile of Smad4-deficient CTLs is similar to TRM

Project description:Transforming growth factor β (TGFβ) is a morphogenic protein that augments antiviral immunity by altering the functional properties of pathogen-specific memory CD8 T cells. During infection, TGFβ inhibits formation of effector (TEFF) and circulating memory CD8 T cells, while encouraging tissue-resident memory CD8 T cells (TRM) to settle in peripheral tissues. SMAD proteins are signaling intermediates that are used by members of the TGF cytokine family to modify gene expression. Using RNA-sequencing we determined that SMAD4 altered the transcriptional profile of antiviral CTLs during respiratory infection. Our data show that SMAD4 and TGFβ use alternate signaling pathways to cooperatively regulate a collection of genes that determine whether pathogen-specific memory CD8 T cells localize in peripheral or lymphoid tissues. During infection, SMAD4 acts independently of TGF to inhibit TRM development, while inducing genes that support formation of circulating memory CD8 T cells. The genes that are modulated by SMAD4 include several homing receptors (CD103, KLRG1 and CD62L) and transcription factors (Hobit and EOMES) that support memory formation.

2021-12-22 | GSE151637 | GEO

Altered transcriptional profile of Smad4-deficient CTLs during infection with Listeria

Project description:TGFb is a pleiotropic cytokine which can exert its regulatory effects on differentiation of cytotoxic T lymphocytes (CTLs) and alter their cell fate. Canonical TGFb signaling inhibits the formation of KLRG1+ effector cells and circulating memory cells while inducing the formation of resident memory cells. However, SMAD4 functions contradictory to TGFb where it is required for the formation of KLRG1+ effector cells and circulating memroy cells and actively inhibit the formation of resident memory cells. Using, RNA-Sequencing we identified that Smad4 alters the gene expression profile of pathogen-specific CTLs after intranasal infection with Listeria monocytogenes expressing chicken ovalbumin.

2022-10-04 | GSE214599 | GEO

Altered transcriptional profile of Smad4-deficient CTLs during infection with Listeria

Project description:Altered transcriptional profile of Smad4-deficient CTLs during infection with Listeria

| PRJNA886076 | ENA

Yap1 ChIP-seq in Pten/Smad4-deficient mouse prostate cancer cells

Project description:Yap1 is a critical transcription coactivator in the Hippo pathways. However, its target genes are not well defined in prostate cancer cells. To determine the downstream transcriptional targets and pathways of Yap1 in Pten/Smad4-defiicent mouse prostate cancer cells, ChIP-seq was performed in the Pten/Smad4-deficient mouse prostate cancer cells.

2022-12-31 | GSE162747 | GEO

Global gene expression profile of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C

Project description:Febrile temperature enhanced Th17 differentiation in Smad4 SUMOylation-dependent manner. Smad4-deficiency impaired the febrile temperature-enhanced Th17 differentiation. In order to understand how febrile temperature and Smad4 contribute to Th17 pathogenicity, we conducted transcriptional analysis of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C (Day 3).

2020-03-01 | GSE125264 | GEO

Super-killer CTLs are generated by single gene deletion of Bach2

Project description:Bach2 codes for a transcriptional regulator exerting major influences on T cell mediated immune regulation. Effector CTLs derived from in vitro activation of murine CD8+ T cells showed increased proliferative and cytolytic capacity in the absence of BACH2. Before activation, BACH2-deficient CD8+ T cells had a higher abundance of memory and reduced abundance of naïve cells compared to wild-type. CTLs derived from central memory T cells were more potently cytotoxic than those derived from naïve T cells, but even within separated subsets, BACH2-deficiency conferred a cytotoxic advantage. Immunofluorescence and electron microscopy revealed larger granules in BACH2-deficient compared to wild-type CTLs, and proteomic analysis showed an increase in granule content, including perforin and granzymes. Thus, the enhanced cytotoxicity observed in effector CTLs lacking BACH2 arises not only from differences in their initial differentiation state but also inherent production of enlarged cytolytic granules. These results demonstrate how a single gene deletion can produce a CTL super-killer.

2022-09-02 | PXD036457 | Pride

RNA-Seq analysis of Tcf7-deficient and -sufficient lung CD8+ TRM cells after influenza infection

Project description:T cell factor 1 (Tcf1, encoded by Tcf7) promotes the central memory CD8+ T cell (TCM) differentiation and homeostatic proliferation in lymphoid tissues. It remains unclear if and how Tcf1 regulates the CD103high tissue-resident memory CD8+ T cell (TRM) formation in non-lymphoid tissues. Using an influenza A infection mouse model, we collected Tcf7-deficient and -sufficient lung CD8+ TRM cells for RNA sequencing analysis.

2020-03-16 | GSE135309 | GEO

CMV-CTLs scVDJ-RNAseq

Project description:CMV-CTLs scVDJ-RNAseq

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Gene expression profile in platelets of mouse regulated by Smad4 gene

Project description:Mutations of SMAD family member 4 (Smad4) gene caused Hereditary Hemorrhagic Telangiectasia (HHT). It was believed that bleeding disorders were caused by arteriovenous malformation in this syndrome. Although several studies indicated dysfunction of platelets from HHT patient, the role(s) of smad4 in platelet function has not been examined. In this study, using megakaryocyte/platelet-specific Smad4-deficient mice, we investigated the physiological function of Smad4 in platelet activation and the underlying mechanism. Microarray data demonstrated that the level of mRNA for multiple genes changed in Smad4 deficient platelet. For microarray analysis, total mRNA was extracted from washed platelets from Smad4f/f or Smad4M-bM-^HM-^R/M-bM-^HM-^R mice (for each group, n=6). mRNA was labeled and hybridized to Affymetrix Mouse Genome 430 2.0 chips according to manufacturer's instructions (Affymetrix).

2013-01-29 | E-GEOD-43814 | biostudies-arrayexpress

CMV-CTLs scVDJ-RNAseq

Project description:We conducted immune- and RNA-sequencing of HLA-A24-restricted CMVpp65-specific CTLs to better understand the immune reconstitution of CMV-CTLs after allo-HCT. To the best of our knowledge, this is the first report on the features of TCRβ-CDR3, diversity, and GEP of HLA-A24 CMV-CTLs according to the CMV-reactivation pattern among recipients after allo-HCT. In addition, we further sought to demonstrate homogeneity or heterogeneity according to individual CTL clones using single-cell RNA-sequencing technology.

2021-01-01 | GSE156841 | GEO

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