Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeting Treg cells with GITR activation alleviates resistance to immunotherapy in murine glioblastomas

ABSTRACT: Targeting Treg cells with GITR activation alleviates resistance to immunotherapy in murine glioblastomas

PROVIDER: PRJNA705184 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13795846_1.fastq.gz	Fastqsanger.gz
	SRR13795846_2.fastq.gz	Fastqsanger.gz
	SRR13795847_1.fastq.gz	Fastqsanger.gz
	SRR13795847_2.fastq.gz	Fastqsanger.gz
	SRR13795848_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 56

Similar Datasets

Targeting Treg cells with GITR activation alleviates resistance to immunotherapy in murine glioblastomas

Project description:Immune checkpoint blockers (ICBs) have failed in all phase III glioblastoma (GBM) trials. Here, we show that regulatory T (Treg) cells play a key role in GBM resistance to ICBs in experimental gliomas. Targeting glucocorticoid-induced TNFR-related receptor (GITR) in Treg cells using an agonistic antibody (αGITR) promotes CD4 Treg cell differentiation into CD4 effector T cells, alleviates Treg cell-mediated suppression of anti-tumor immune response, and induces potent anti-tumor effector cells in GBM. The reprogrammed GBM-infiltrating Treg cells express genes associated with a Th1 response signature, produce IFNγ, and acquire cytotoxic activity against GBM tumor cells while losing their suppressive function. αGITR and αPD1 antibodies increase survival benefit in three experimental GBM models, with a fraction of cohorts exhibiting complete tumor eradication and immune memory upon tumor re-challenge. Moreover, αGITR and αPD1 synergize with the standard of care treatment for newly-diagnosed GBM, enhancing the cure rates in these GBM models.

2021-03-27 | GSE167746 | GEO

Targeting Treg cells with GITR activation alleviates resistance to immunotherapy in murine glioblastomas.

| S-EPMC8113440 | biostudies-literature

mRNA expression in CD4+ CD25+ GITR+ regulatory T cells from WT and Bach2 KO mice

Project description:Bach2 regulates homeostasis of foxp3+ regulatory T cells and protects against fatal lung disease in mice. Cells from WT and Bach2 KO spleen were isolated. CD4+ CD25+ GITR+ (Treg) cells were sorted by FACS sorting. Total RNAs were extracted from sorted Treg cells using by Rneasy Kit (Qiagen).

2013-11-14 | E-GEOD-52337 | biostudies-arrayexpress

Antibody-mediated blockade of the IL-23 receptor destabilizes intratumoral regulatory T cells and enhances immunotherapy

Project description:Regulatory T cells (Treg) can impede anti-tumor immunity and currently represent a major obstacle to effective cancer immunotherapy. Targeting tumor-infiltrating regulatory Treg while sparing systemic Treg represent optimal approaches to this problem. Here, we provide evidence that the interleukin 23 receptor (IL23R) expressed by tumor-infiltrating Treg promotes suppressive activity. Disruption of the IL23R results in increased responsiveness of destabilized Treg to the IL-12 cytokine, production of g-interferon (IFNg) and recruitment of CD8 T cells that inhibit tumor growth. Since the Treg destabilization pathway that is initiated by IL23R blockade is distinct and independent from the destabilization pathway coupled to Glucocorticoid-Induced TNFR-Related protein (GITR) activation, we examined the impact of coordinate induction of the two destabilization pathways on anti-tumor immune responses. Combined GITR and IL23R antibody treatment of mice inoculated with MC38 tumors resulted in robust and synergistic anti-tumor responses. These findings indicate that delineation of independent Treg destabilization pathways may allow improved approaches to the development of combination immunotherapy for cancers.

2022-05-02 | GSE197287 | GEO

Gene expression based outcome of CT-26 tumor in C57/BL6 mice after treatment with anti-PD-1 antibody, GITR-L, combination or Bispecific molecules

Project description:Co-stimulatory receptors such as GITR play key roles in regulating the effector functions of T cells. Agonistic anti-GITR antibodies have been investigated as a cancer immunotherapy with demonstrated efficacy in pre-clinical models. In human clinical trials, however, GITR agonist antibodies have shown limited therapeutic effect which may be due to a suboptimal receptor clustering-mediated signaling. To overcome this potential limitation, a rational protein engineering approach is needed to optimize GITR agonist-based immunotherapies. Here we show a novel bispecific molecule consisting of an anti-PD-1 antibody fused with a multimeric GITR ligand (anti-PD-1-GITR-L) that induces a PD-1-dependent and FcγR-independent GITR clustering, resulting in an enhanced activation, proliferation, and memory differentiation of primed antigen-specific GITR+PD-1+ T cells. The anti-PD-1-GITR-L bispecific is a PD-1 directed GITR-L construct that has a different mechanism of action (MoA) than the co-administration of anti-PD-1 plus GITR-L and demonstrated a dose-dependent immunologically driven tumor growth inhibition in syngeneic, genetically engineered and xenograft humanized mouse tumor models. Combination of anti-PD-1-GITR-L with TGFβ inhibition or chemotherapy (gemcitabine), respectively, resulted in tumor remission in immunogenically cold and checkpoint blockade resistant mouse models. Dose-dependent correlations between target saturation and Ki67 and TIGIT up-regulation on memory T cells have been observed following a single dose of anti-PD-1-GITR-L bispecific in mice and non-human primates. Anti-PD-1-GITR-L thus represents a novel bispecific approach for directing GITR agonism for cancer immunotherapy.

2021-12-20 | GSE189359 | GEO

GITR and GITRL protects non-epithelioid mesothelioma cells from radiation

Project description:GITR and GITRL overexpress in sarcomatoid mesotelioma cells than epithelioid subtype, and cisplatin or radiation results an increase of GITR and GITRL expression on tumor cells. After sorting CRL9546 cells into GITR+(R), GITRL+(L), and GITR-/GITRL- (DN) cell populations. Three cell subsets were labelled as ligand positive L1, L2, L3, receptor positive R1, R2, R3, and double negative DN1, DN2, DN3. In total: 9 samples. RNA was extracted to run Affymetrix microarray.

2021-11-02 | E-MTAB-10647 | biostudies-arrayexpress

Very low tumor mutation burden identifies inflamed recurrent glioblastomas responsive to cancer immunotherapy

Project description:Very low tumor mutation burden identifies inflamed recurrent glioblastomas responsive to cancer immunotherapy

| PRJNA668405 | ENA

Predictive Biomarkers for the Responsiveness of Recurrent Glioblastomas to Activated Killer Cell Immunotherapy

Project description:Predictive Biomarkers for the Responsiveness of Recurrent Glioblastomas to Activated Killer Cell Immunotherapy

| PRJNA857011 | ENA

Very low tumor mutation burden identifies inflamed recurrent glioblastomas responsive to cancer immunotherapy

Project description:Very low tumor mutation burden identifies inflamed recurrent glioblastomas responsive to cancer immunotherapy

| PRJNA668404 | ENA

RORγt -expressing FOXP3+ skin-resident Treg cells derived from the periphery in Allergen-Specific Immunotherapy

Project description:The study explored the impact of Specific Immunotherapy on patients with Atopic Dermatitis sensitized to house dust mites by analyzing the transcriptomes of T regulatory cells before and after treatment. Result found that effective SIT is associated with distinct gene expression changes in Treg cells, particularly increased expression of Treg markers and RORC, a gene linked to immune regulation. These results indicate that successful SIT may enhance the function of Treg cells expressed RORC and help restore immune balance in these patients.

2024-05-01 | GSE252205 | 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