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Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases [Foxp3Cre Myd88fl/fl]

ABSTRACT: Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases [Foxp3Cre Myd88fl/fl]

PROVIDER: PRJNA645366 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12192786_1.fastq.gz	Fastqsanger.gz
	SRR12192786_2.fastq.gz	Fastqsanger.gz
	SRR12192787_1.fastq.gz	Fastqsanger.gz
	SRR12192787_2.fastq.gz	Fastqsanger.gz
	SRR12192788_1.fastq.gz	Fastqsanger.gz

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Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases [Foxp3Cre Myd88fl/fl]

Project description:Upregulate and stabilize Foxp3 expression in Treg are essential for manipulating Treg cell function and immune homeostasis. Here, we examined the potential role and mechanism of gp96 protein in regulating FoxP3 transcription and Treg activation in vivo.

2020-07-11 | GSE154172 | GEO

Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases [FFoxp3-GFP-hCre]

2020-07-11 | GSE154173 | GEO

Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases

Project description:Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases

| PRJNA645364 | ENA

Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases [FFoxp3-GFP-hCre]

Project description:Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases [FFoxp3-GFP-hCre]

| PRJNA645367 | ENA

Non-classical action of Ku70 promotes Treg suppressive function through a FOXP3-dependent mechanism in lung adenocarcinoma

Project description:To explore the role of Ku70 in Treg cell biology, we isolated conventional T cells (Tconv) and regulatory T cells (Treg) from Foxp3Yfp-cre mice and performed Ku70 ChIP-seq. Furthermore, to investigate the impact of Ku70 deficiency on Foxp3 binding patterns, we sorted Treg cells from Foxp3Cre (WT) and Xrcc6fl/fl;Foxp3Cre (KO) mice and conducted Foxp3 ChIP-seq. These analyses revealed that Ku70 forms a complex with FOXP3, which supports FOXP3 transcriptional activity.

2024-11-04 | GSE278950 | GEO

Inhibition of p300 impairs Foxp3+ T-regulatory cell function and promotes anti-tumor immunity

Project description:Foxp3+ T-regulatory (Treg) cells maintain immune homeostasis and limit autoimmunity, but can also curtail host responses to cancers. Tregs are therefore promising targets to enhance anti-tumor immunity. Histone/protein acetyltransferases (HATs) promote chromatin accessibility, gene transcription and the function of multiple transcription factors and non-histone proteins. We found that conditional deletion or pharmacologic inhibition of one specific HAT, p300, in Foxp3+ Tregs, increased TCR-induced apoptosis in Tregs, impaired Treg suppressive function and iTreg peripheral conversion, and limited tumor growth in immunocompetent, but not in immunodeficient, hosts. Our data demonstrate that p300 is important for Foxp3+ Treg function and homeostasis in vivo and in vitro, and identify a novel mechanism to diminish Treg function without overtly impairing effector Tcell responses or inducing autoimmunity. Collectively, these data suggest a new approach for cancer immunotherapy. RNA from three independent samples from magnetically separated CD4+CD25+ Treg of fl-p300/Foxp3cre mice, compared to wild type (Foxp3cre) control (all C57Bl/6 background).

2013-08-18 | E-GEOD-47989 | biostudies-arrayexpress

Two Histone/Protein Acetyltransferases, CBP and p300, Are Indispensable for Foxp3+ T-regulatory Cell Development and Function

Project description:T-regulatory (Treg) cells are important to immune homeostasis, and Treg cell deficiency or dysfunction leads to autoimmune disease. An histone/protein acetyltransferase (HAT), p300, was recently found important for Treg function and stability, but further insights into the mechanisms by which p300 or other HATs affect Treg biology are needed. Here we show that CBP, a p300 paralog, is also important in controlling Treg function and stability. Thus, while mice with Treg-specific deletion of CBP or p300 developed minimal autoimmune disease, the combined deletion of CBP and p300 led to fatal autoimmunity by 3-4 weeks of age. The effects of CBP and p300 deletion on Treg development are dose-dependent, and involve multiple mechanisms. CBP and p300 cooperate with several key Treg transcription factors that act on the Foxp3 promoter to promote Foxp3 production. CBP and p300 also act on the Foxp3 CNS2 region to maintain Treg stability in inflammatory environments by regulating pCREB function and GATA3 expression, respectively. Lastly, CBP and p300 regulate the epigenetic status and function of Foxp3. Our findings provide insights into how HATs orchestrate multiple aspects of Treg development and function, and identify overlapping but also discrete activities for p300 and CBP in control of Treg cells. RNA from three independent samples from magnetically separated CD4+CD25+ Treg of fl-p300/Foxp3cre mice and fl-CBP/Foxp3cre, compared to wild type (Foxp3cre) control (all C57Bl/6 background).

2014-08-12 | E-GEOD-60318 | biostudies-arrayexpress

Expression profiling of tumor-infiltrating CD4+ FOXP3- conventional T cells from tumors of wildtype and Foxp3-Cre x CK2b-fl/fl mice

Project description:Analysis of tumor-infiltrating CD4+ FOXP3- conventional T cells from tumors of Rosa26-RFP x Csnk2bfl/fl mice (wildtype) and Rosa26-RFP x Csnk2bfl/fl x Foxp3-Cre mice.

2025-07-30 | GSE237146 | GEO

Critical Requirement of the DNA Methyltransferase, Dnmt1, for the Development and Function of Foxp3+ Regulatory T Cells

Project description:We investigated the role of DNMT1 in immune homeostasis by generating mice lacking DNMT1 in Foxp3+ T-regulatory (Treg) cells. These mice showed decreased peripheral Foxp3+ Tregs, complete loss of Foxp3+ Treg suppressive functions in vitro and in vivo, and died from autoimmunity by 3-4 weeks unless they received perinatal transfer of wild-type Tregs that prolonged their survival. Methylation of CpG-sites in the TSDR region of Foxp3 was unaffected by DNMT1 deletion, but microarray revealed more >500 proinflammatory and other genes were upregulated in DNMT1-/- Tregs. CD4-Cre-mediated DNMT1 deletion showed inability of conventional T cells to convert to Foxp3+ Treg under appropriate polarizing conditions. Hence, DNMT1 is absolutely necessary for maintenance of the gene program required for normal Treg development and function. RNA from three independent samples of magnetically separated CD4+CD25+ Treg of fl-DNMT1/Foxp3cre mice, compared to wild type (C57BL6) control

2013-04-21 | E-GEOD-27434 | biostudies-arrayexpress

Identification of potential CCDC134 interactors by immunoprecipitation and LC-MS analysis

Project description:Our data indicate that CCDC134 plays a critical role in regulating the biogenesis of Toll-like receptors (TLRs). To gain deeper insights into the molecular mechanisms through which CCDC134 mediates TLR regulation, we sought to identify potential binding partners using interaction proteomics. Mass spectrometry analysis of Flag-CCDC134 immunoprecipitates from stably reconstituted CCDC134 knockout CAL-1 cells provided a better understanding of the interaction landscape associated with CCDC134. Notably, among the identified proteins, the TLR chaperone Gp96 emerged as one of the strongest binding partners. We further validated that CCDC134 interacts with Gp96 and is essential for its proper folding and stability. Consequently, loss of CCDC134 impairs the folding, maturation, and trafficking of TLRs.

2024-11-14 | PXD053008 | Pride

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