Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation (whole genome enzymatic methylation sequencing)

ABSTRACT: The mechanisms behind survival of autoimmune CD4 T cells during chronic stimulation are unclear. Examining early time-points during T cell priming showed that activation of autoimmune CD4 T cells in the absence of infectious signals allowed maintenance of TCF1 expression, albeit at reduced levels. Tcf7 locus was epigenetically modified in circulating autoimmune CD4 T cells, suggesting a pre-programmed de novo methylation of the locus in early stages of autoimmune CD4 T cell differentiation which mirrored the epigenetic profile of recently recruited CD4 CD62L+ T cells in the tissue. Collectively, the data presented here show that the unique environment during autoimmune CD4 T cell priming allows T cells to finetune TCF1 expression to maintain long-term survival and function.

ORGANISM(S): Mus musculus

PROVIDER: GSE273728 | GEO | 2024/10/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation

Project description:The mechanisms behind survival of autoimmune CD4 T cells during chronic stimulation are unclear. Examining early time-points during T cell priming showed that activation of autoimmune CD4 T cells in the absence of infectious signals allowed maintenance of TCF1 expression, albeit at reduced levels. Tcf7 locus was epigenetically modified in circulating autoimmune CD4 T cells, suggesting a pre-programmed de novo methylation of the locus in early stages of autoimmune CD4 T cell differentiation which mirrored the epigenetic profile of recently recruited CD4 CD62L+ T cells in the tissue. Collectively, the data presented here show that the unique environment during autoimmune CD4 T cell priming allows T cells to finetune TCF1 expression to maintain long-term survival and function.

2024-10-12 | GSE272660 | GEO

Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation (NOD)

2024-10-12 | GSE273633 | GEO

Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation

Project description:Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation

| PRJNA1137917 | ENA

Formation and fate of stem-cell like Tcf7+ CD8+ T cells during a primary immune response to viral infection [scRNA-seq]

Project description:In response to infection, naïve CD8+ T cells (Tn) expand and differentiate into short-lived terminal effector (Tte) cells, which eliminate infected cells, or into central memory (Tcm) cells, which persist following pathogen clearance and mediate protection against re-infection thanks to their stem cell-like properties. The stage-specific signals required for the cell fate changes have remained incompletely understood. Here we find that Tn cells, which express the transcription factor Tcf1 (Tcf7), yield Tcf1+ cells, which retain stem-like potential throughout the primary response and which quantitatively yield Tcf1+ Tcm cells following pathogen clearance. However, only the Tcf1+ cells present during priming are competent to yield Tcf1- Tte cells. Priming commits cells to undergo multiple divisions while maintaining Tcf1 expression. The presence of type I interferon during the division, rather than the priming phase suppresses Tcf1 expression. Tcf1 loss results in the stable loss of stemness, an event that precedes the stable acquisition of a Tte state. Thus, inflammatory cytokines drive Tte differentiation from dividing Tcf1+ cells, which are prone to become Tcm cells.

2023-11-06 | GSE221968 | GEO

Formation and fate of stem-cell like Tcf7+ CD8+ T cells during a primary immune response to viral infection [ATAC-seq]

2023-11-06 | GSE221967 | GEO

Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation (NOD)

Project description:Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation (NOD)

| PRJNA1142535 | ENA

Impact of Tcf1 and Lef1 deficiency on histone marks and Tcf1 binding in CD8 T cells

Project description:Comparison of epigenome and Tcf1 occupancy between control and Tcf1/Lef1-deficient CD8 T cells Control mice or those are deficient for Tcf1 and Lef1 transcription factors (deleted by CD4-Cre) were used to isolate thymocytes. The thymocytes were surface-stained to identify TCRbeta high, CD69â, CD24â CD8+ subsets. These cells were sorted for ChIPseq analysis of various histone marks. Control mice or those are deficient for Tcf1 (deleted by CD4-Cre) were used to isolate thymocytes. The splenocytes were surface-stained to identify TCRbeta high, CD8+ subsets. These cells were sorted for ChIPseq analysis of Tcf1 binding locations.

2016-02-12 | E-GEOD-73239 | biostudies-arrayexpress

Inverted chromatin immunoprecipitation identifies Tcf1 as a negative regulator of Foxp3 expression

Project description:Regulatory T (Treg) cells are important regulators of the immune system and have versatile functions for the homeostasis and repair of tissues. They express the forkhead box transcription factor Foxp3 as a lineage-defining protein. In mature Treg cells, the Foxp3 core promoter is unmethylated indicating that this area could harbor a transcription factor complex to initiate or repress gene expression, respectively. We used an unbiased method to identify Foxp3-promoter-binding transcription factors (TFs) by inverted chromatin immunoprecipitation (IP) followed by quantitative mass spectrometry. We identified several candidate factors which showed Foxp3-promoter suppressive capacity, one of which was T-cell factor 1 (Tcf1). Using viral overexpression and CRISPR/Cas knockout studies, we identified Tcf1 as a repressor of Foxp3 expression in primary conventional CD4 T cells (Tconv). In Tcf1-deficient animals, increased levels of Foxp3intermediateCD25negative T cells were identified in secondary lymphoid tissues, implicating that Tcf1 protects Foxp3-negative T cells from inadvertent Foxp3 expression.

2020-05-26 | PXD018764 | Pride

CD4+ T cells treated with TNFalpha blocking agents during activation.

Project description:Objective. TNF? is a potent pro-inflammatory cytokine playing a pivotal role in several autoimmune diseases. Neutralizing TNF? inhibits T cell proliferation and IFN? production, and enhances suppressive capacity of regulatory T cells (Treg). Little is known about the mechanism of TNF? blocking agents on naïve T cell differentiation. Methods. Naïve CD4+ T cells were activated by dendritic cells (DC) in presence or absence of anti-TNF? agents. T cell polarization and activation was assessed during T cell differentiation. In addition, whole genome gene expression analysis was performed on anti-TNF?-treated T cells. Results. Neutralizing TNF? during priming of naïve CD4+ T cells by DC favors development of IL-10+ T helper (Th) cells at the expense of IFN? induction. TNF? inhibits IL-10 via TNFRII, which becomes expressed after naïve T cell activation. While initial CD4+ T cell activation was not affected, neutralization of TNF? negatively affected later stages of T cell priming by counteracting full T cell activation and survival. Whole genome gene expression analysis revealed a regulatory gene profile of anti-TNF?-treated T cells. Indeed, neutralizing TNF? during naïve T cell priming enhanced the suppressive function of anti-TNF?-treated T cells. Conclusion. Inhibition of TNF?–TNFRII interaction affects late stage effector T cell development and shifts the balance of Th cell differentiation towards IL-10 expressing regulatory T cells, which may be one of the beneficial mechanisms in TNF? blocking therapies. Naïve CD4+ T cells were CFSE labeled and co-cultured for 13 days with allogeneic dendritic cells in the presence or absence of anti-TNF? agents. After 13 days, the CFSElow T cells were FACS sorted. Samples were generated from three independent donors.

2014-06-25 | E-GEOD-42812 | biostudies-arrayexpress

Genome-wide maps of Tcf1 binding locations in splenic CD8 T cells.

Project description:We mapped genome-wide Tcf1 binding locations in mature CD8 T cells to identify its direct target genes. This experiment aims to identify genome-wide binding locations for Tcf1 transcription factor in mature CD8 T cells. The CD8 T cells were isolated from wild-type C57BL/6 mice by negative selection. The chromatin fragments were immunoprecipitated by an anti-Tcf1 antiserum or control rabbit serum (without immunization). The immunoprecipitated fragments were then used in high throughput sequencing. Data processing then revealed >3000 high-confidence Tcf1 binding peaks across the CD8 T cell genome. One important finding is that Tcf1 binds directly to Cd4 gene silencer, and thus explain its important role in suppressing the CD4 coreceptor in mature CD8 T cells.

2014-03-05 | E-GEOD-52070 | biostudies-arrayexpress

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