Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparison of gene profile of WT, STAT3 KO donor T cells in the spleen of allogenetic HCT mouse recepients

ABSTRACT: Comparison of gene profile of WT, STAT3 KO donor T cells in the spleen of allogenetic HCT mouse recepients

PROVIDER: PRJNA885813 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21768906.fastq.gz	Fastqsanger.gz
	SRR21768907.fastq.gz	Fastqsanger.gz
	SRR21768908.fastq.gz	Fastqsanger.gz
	SRR21768909.fastq.gz	Fastqsanger.gz
	SRR21768910.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Comparison of gene profile of WT, STAT3 KO and STAT3koPD-1ko donor T cells in the liver of allogenetic HCT mouse recepients

Project description:Comparison of gene profile of WT, STAT3 KO and STAT3koPD-1ko donor T cells in the liver of allogenetic HCT mouse recepients

| PRJNA885777 | ENA

Comparison of gene profile of WT, STAT3 KO donor T cells in the spleen of allogenetic HCT mouse recepients

Project description:We injected Thy1.2+ T cells from WT or STAT3ko C57BL/6 mice with T cell-depleted bone marrow cells from WT C57BL/6 mice into WT BALB/c recipients to establish acute GVHD model.

2023-08-08 | GSE214529 | GEO

Transcriptome profile of HCT 116p53-/- and HCT 116p53-/- RPL3 KO during Actinomycin (Act D) treatment

Project description:To analyse gene expression differences between HCT 116p53-/- and HCT 116p53-/- RPL3 KO and/or during Actinomycin treatment (Act D)

2020-04-13 | GSE145807 | GEO

Donor non-classical monocytes recruit recipient classical monocytes from the spleen by activating donor alveolar macrophages

Project description:Primary Graft Dysfunction (PGD) is the predominant cause of early graft loss following lung transplantation. We recently demonstrated that donor pulmonary intravascular non-classical monocytes (NCM) initiate neutrophil recruitment. Simultaneously, host-origin classical monocytes (CM) are mobilized from the spleen and, upon entry into the allograft, permeabilize the vascular endothelium to allow neutrophil extravasation necessary for PGD. Here, we show that CCL2-CCR2 axis is necessary for CM recruitment. Surprisingly, although intravital imaging and multichannel flow cytometry revealed that pharmacological or genetic depletion of donor NCM abrogated CM recruitment, single-cell RNAseq identified donor alveolar macrophages (AM) as predominant CCL2 secretors. Unbiased transcriptomic analysis of human and murine tissues combined with murine knockouts and chimeras indicated that while IL1β was secreted by multiple cell lineages, donor NCM were responsible for the early activation of AM and CCL2 release. IL1β production by NCM was NLRP3 inflammasome-dependent and inhibited by donor treatment using a clinically approved sulphonylurea, Glyburide. Production of CCL2 in the donor AM occurred through IL1R-dependent activation of PKC and NFκB-pathway. Accordingly, we show that IL1β-dependent paracrine interaction between donor NCM and AM leads to recruitment of host AM necessary for PGD. Since depletion of donor NCM, IL1β or IL1R antagonism, and inflammasome inhibition, abrogated recruitment of CM as well as PGD and are feasible using FDA-approved compounds, our findings have potential for immediate clinical translation.

2024-02-01 | GSE166679 | GEO

Donor non-classical monocytes recruit recipient classical monocytes from the spleen by activating donor alveolar macrophages

Project description:Donor non-classical monocytes recruit recipient classical monocytes from the spleen by activating donor alveolar macrophages

| PRJNA701602 | ENA

Isolation of spleen lymph during leukemia development

Project description:Here we asked whether infiltration of leukemic blasts initiated a response that could be detected in the interstitial fluid phase of the spleen in a rat model known to mimic human acute myeloid leukemia (AML). By cannulating efferent lymphatic vessels, we were able to monitor the response of the spleen microenvironment during leukemia development. Flow cytometric analysis of lymphocytes isolated from spleen lymph showed increased STAT3 and CREB signaling, and proteins related to these pathways were identified with a different profile in leukemic when compared with control spleen lymph. Additionally, SPARC-like 1 protein, recently identified as a promoter of AML cell growth and a biomarker of patient outcome, was locally produced in the spleen and upregulated in the leukemic setting. Thus, interstitial fluid, and its surrogate efferent lymph, can be used to provide unique information about spleen responses and substances released to the general circulation during leukemia development.

2023-06-23 | PXD011399 | Pride

A spatial transcriptomics study of splenic marginal zone lymphomas (SMZL) and spleen healthy donor

Project description:Purpose: Spatial transcriptomics was used to characterize in depth splenic samples obtained from splenic marginal zone lymphomas Methods: 4 frozen samples of spleen from SMZL patients, and 1 healthy donor were selected and thawed for performing a 10X genomics Visium Spatial assay. Results: Tumor cells formed mainly patient specific-B cell clusters, while T-cells from the 3 patients and healthy donors clustered together. Conclusion: Single RNA-Seq unveils inter- and intra-patient heterogeneity.

2024-09-17 | GSE228056 | GEO

Comparison of gene profile of WT, STAT3 KO and STAT3koPD-1ko donor T cells in the liver of allogenetic HCT mouse recepients

Project description:We injected Thy1.2+ T cells from WT or STAT3ko or STAT3koPD-1ko C57BL/6 mice with T cell-depleted bone marrow cells from WT C57BL/6 mice into WT BALB/c recipients to establish acute GVHD model.

2023-08-08 | GSE214506 | GEO

Transcriptome profile of HCT 116p53-/- and HCT 116p53-/- RPL3 KO during Actinomycin (Act D) treatment

Project description:Transcriptome profile of HCT 116p53-/- and HCT 116p53-/- RPL3 KO during Actinomycin (Act D) treatment

| PRJNA608302 | ENA

Galectin-3 expression in donor T cells reduces GvHD severity and lethality after allogeneic hematopoietic cell transplantation

Project description:Abundant donor cytotoxic T cells that attack normal host organs remain a major problem for patients receiving allogeneic hematopoietic cell transplantation (Allo-HCT). Despite an increase in our knowledge of the pathobiology of acute graft versus host disease (aGvHD), the mechanisms regulating the proliferation and function of donor T cells remain unclear. Here, we show that activated donor T cells express galectin-3 (Gal-3) after allo-HCT. In both major and minor histocompatibility–mismatched models of murine aGvHD, expression of Gal-3 is associated with decreased T cell activation and suppression of the secretion of effector cytokines including IFN-γ and GM-CSF. Mechanistically, Gal-3 results in activation of NFAT signaling which can induce T cell exhaustion. Gal-3 overexpression in human T cells prevents severe disease by suppressing cytotoxic T cells in xenogeneic aGvHD models. Together these data identify the Gal-3-dependent regulatory pathway in donor T cells as a critical component of inflammation in aGvHD.

2023-03-13 | GSE225756 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data