Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile of effector Treg cells isolated from spleens and tumors of tumor-bearing mice

ABSTRACT: A majority of effector Treg cells (eTregs) that are abundant in many types of tumors are marked by the expression of Blimp1. However, the specific impact of Blimp1+ eTregs on, and mechanisms of action within, tumors remain unknown. To better understand the role of Blimp1 in the regulation of eTreg function in the tumor immunity, we profiled the differential gene expression in Blimp1-deficient eTregs compared to WT control eTregs from tumor-bearing mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE178132 | GEO | 2021/11/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

miR-15/16 clusters restrict effector Treg cell differentiation and function

Project description:Effector regulatory T cells (eTregs) exhibit distinct homeostatic properties and superior suppressor capacities pivotal for controlling immune responses mediated by their conventional T cell counterpart. While the role of microRNAs (miRNAs) in Tregs has been well-established, how miRNAs regulate eTregs remains poorly understood. Here, we demonstrate that miR-15/16 clusters act as key regulators in limiting eTreg responses. Loss of miR-15/16 clusters leads to increased eTreg frequencies with enhanced suppressor function. Consequently, mice with Treg-specific ablation of miR-15/16 clusters display attenuated immune responses during neuroinflammation and upon both infectious and non-infectious challenges. Mechanistically, miR-15/16 clusters exert their regulatory effect in part through repressing IRF4, a transcription factor essential for eTreg differentiation and function. Moreover, miR-15/16 clusters also directly target neuritin, an IRF4-dependent molecule, known for its role in Treg-mediated regulation of plasma cell responses. Together, we identify an miRNA family that controls an important Treg subset and further demonstrate that eTreg responses are tightly regulated at both transcriptional and posttranscriptional levels.

2023-07-21 | GSE225737 | GEO

Neoadjuvant PARPi or Chemotherapy in Ovarian Cancer Informs Targeting Effector Treg Cells for Homologous-Recombination-Deficient Tumors [Singleron scRNA-seq]

Project description:Homologous recombination deficiency (HRD) is prevalent in cancer, sensitizing tumor cells to PARP inhibition. However, the impact of HRD and related therapies on the tumor microenvironment (TME) remains elusive. Our study generates single-cell gene expression and T-cell receptor profiles, along with validatory multimodal datasets from > 100 high-grade serous ovarian cancer (HGSOC) samples, primarily from a phase II clinical trial (NCT04507841). Neoadjuvant monotherapy with the PARP inhibitor niraparib achieves impressive 62.5% and 73.6% response rates per RECIST v1.1 and GCIG CA125, respectively. We identify effector regulatory T cells (eTreg) as key responders to HRD and neoadjuvant therapies, co-occurring with other tumor-reactive T cells, particularly terminally exhausted CD8+ T cells (Tex). TME-wide interferon signaling correlates with cancer cells upregulating MHC-II and co-inhibitory ligands, potentially driving Treg and Tex fates. Depleting eTregs in HRD mouse models, with or without PARP inhibition, significantly suppresses tumor growth without observable toxicities, underscoring the potential of eTreg-focused therapeutics for HGSOC and other HRD-related tumors.

2024-07-08 | GSE269793 | GEO

Neoadjuvant PARPi or Chemotherapy in Ovarian Cancer Informs Targeting Effector Treg Cells for Homologous-Recombination-Deficient Tumors [Singleron scTCR-seq]

2024-07-08 | GSE222555 | GEO

Neoadjuvant PARPi or Chemotherapy in Ovarian Cancer Informs Targeting Effector Treg Cells for Homologous-Recombination-Deficient Tumors [bulk TCR-seq]

2024-07-08 | GSE222554 | GEO

Neoadjuvant PARPi or Chemotherapy in Ovarian Cancer Informs Targeting Effector Treg Cells for Homologous-Recombination-Deficient Tumors [10x scRNA-seq]

2024-07-08 | GSE222556 | GEO

Gene expression profile of effector Treg cells isolated from spleens and tumors of tumor-bearing mice

Project description:Gene expression profile of effector Treg cells isolated from spleens and tumors of tumor-bearing mice

| PRJNA737439 | ENA

IL-23 stabilizes an effector Treg program in the tumor microenvironment

Project description:Regulatory T cells (Tregs) are crucial for the maintenance of immune tolerance and restrict immunopathology during inflammation, yet they limit efficient anti-tumor immunity in the tumor microenvironment (TME). Effector Tregs (eTregs) are thought to be the cellular subset equipped with the strongest immunosuppressive and cancer promoting properties. Here we found by in preclinical cancer models, that Treg specific deletion of IL23R reduces tumor growth. Using heterozygous conditional knock-out mice in which Il23r KO and Il23r WT Tregs coexist in the same tumor microenvironment, we found that IL-23 sensing represents a crucial signal driving the maintenance and stabilization of eTregs involving the transcription factor Foxp3.

2024-05-31 | GSE224072 | GEO

Interleukin-2 receptor signaling acts as a checkpoint that shapes the distribution of regulatory T cell subsets (scRNA-Seq)

Project description:Regulatory T cells (Tregs) require IL-2 for survival in the periphery, yet how IL-2 shapes Treg heterogeneity remains poorly defined. Here we found that inhibition of IL-2R signaling in post-thymic Tregs leads to a preferential early loss of central Tregs (cTregs). Gene expression of cTregs was more dependent on IL-2R signaling than effector Tregs (eTregs). Unexpectedly, ablation of IL-2R signaling in cTregs resulted in increased proliferation, expression of eTreg genes, and enhanced capacity to develop into eTregs. These findings indicate that physiological amounts of IL-2 act as a checkpoint to maintain cTreg homeostasis and tolerance while restraining their development into eTregs. Nevertheless, direct evaluation of eTregs revealed that loss of IL-2R signaling alters the distribution of eTreg subsets, with increased IFNgR1+ eTregs and CXCR5+ PD-1+ T follicular regulatory (TFR) cells but decreased intestinal RORgt+ TR17 cells. Thus, IL-2R signaling also shapes the development of specialized eTregs subsets.

2024-10-18 | GSE268022 | GEO

Interleukin-2 receptor signaling acts as a checkpoint that shapes the distribution of regulatory T cell subsets (RNA-Seq)

2024-10-18 | GSE268021 | GEO

Distinct Vps34-orchestrated signaling processes dictate the transitional heterogeneity and functional adaptation of effector Treg cells [scRNAseq]

Project description:Emerging evidence highlights regulatory T cell (Treg) heterogeneity in lymphoid and non-lymphoid tissues, but we have limited understanding of context-dependent functions and spatiotemporal regulators of heterogenous Treg states, especially during perinatal life when immune tolerance is established. Using single-cell transcriptomics profiling and experimental validations, we revealed that Vps34 is essential for orchestrating effector Treg (eTreg) transitional heterogeneity during perinatal life. We found that loss of Vps34 reduced terminal eTreg accumulation in lymphoid tissues, associated with decreased generation of Treg cells in non-lymphoid tissues and development of an early-onset autoimmune disease. After perinatal life, Vps34-deficient eTreg accumulation was further impaired due to reduced survival, highlighting temporal regulation of eTreg heterogeneity and maintenance by Vps34. Accordingly, inhibition of Vps34 in mature Treg cells also disrupted immune homeostasis but boosted anti-tumor immunity. Mechanistically, multiomics profiling approaches uncovered that Vps34-orchestrated transcriptional and epigenetic remodeling promotes terminal eTreg programming. Further, via genetic deletion of the Vps34-interacting proteins Atg14 or Uvrag in Treg cells, we established that autophagy (via Atg14) but not endocytosis (via Uvrag) was required for the overall survival, but not transitional heterogeneity, of eTreg cells. Accordingly, mice with Treg-specific deletion of Atg14, but not Uvrag, had moderately disrupted immune homeostasis and reduced tumor growth, with Vps34 and Atg14-dependent gene signatures also being elevated in intratumoral Treg cells from human cancer patients. Collectively, our study reveals distinct Vps34-orchestrated signaling events that temporally regulate eTreg heterogeneity and functional adaptation and the pathophysiological outcomes on autoimmunity versus anti-tumor immunity.

2025-02-25 | GSE283258 | 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