Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Paired VDJ and transcriptome single cell sequencing in LMP2 multimer-positive human T cells treated with anti-PD-L1 and anti-TIM3 antibodies.

ABSTRACT: We report the change in gene expression profile paired to clonotype profiling in single cells from LMP2 multimer-positive human T cells generated following weekly stimulations with antigen-pulsed dendritic cells and subjected or not to PD-L1/TIM3 double blockade.

ORGANISM(S): Homo sapiens

PROVIDER: GSE181682 | GEO | 2024/08/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

TCR beta sequencing in LMP2-positive and LMP2-negative human T cells treated with anti-PD-L1 and anti-TIM3 antibodies.

Project description:We report the change in TCR beta profile of LMP2 multimer-positive and multimer-negative human T cells generated following weekly stimulations with antigen-pulsed dendritic cells and subjected or not to PD-L1/TIM3 double blockade.

2024-08-20 | GSE182537 | GEO

Paired VDJ and transcriptome single cell sequencing in LMP2 multimer-positive human T cells treated with anti-PD-L1 and anti-TIM3 antibodies.

Project description:Paired VDJ and transcriptome single cell sequencing in LMP2 multimer-positive human T cells treated with anti-PD-L1 and anti-TIM3 antibodies.

| PRJNA753016 | ENA

TCR beta sequencing in LMP2-positive and LMP2-negative human T cells treated with anti-PD-L1 and anti-TIM3 antibodies.

Project description:TCR beta sequencing in LMP2-positive and LMP2-negative human T cells treated with anti-PD-L1 and anti-TIM3 antibodies.

| PRJNA756689 | ENA

Tumor-activating IL2 rejuvenates intratumoral TIM3-CD8+T cell responses through targeting TIM3+CD8+T cell

Project description:TIM3, a T-cell inhibitory receptor, is expressed on exhausted T cells in tumor microenvironment (TME). Anti-TIM3 antibody therapy could alleviate the suppression of tumor-infiltrating lymphocytes (TILs) in IL-2 dependent fashion. We hypothesize that high expression of TIM3 and limited IL-2 in TME facilitate immune evasion. To test that, we engineered anti-TIM3-pro-IL2 to selectively deliver IL-2 to TIM3high TILs by TIM3 antibody and reduce its toxicity with a cis delivery mechanism. Since IL-2 could reduce its activity at acidic pH inside TME, we also screened a low pH-selective IL-2 mutein (IL2V2) with enhanced affinity for IL-2Rβ. We then integrated pro-IL-2 into the anti-TIM3 antibodies in two different forms: TIM3-Rα-MMPs-IL2V2 (TIM3-ProIL2V2) as IL-2 release-form vs TIM3-IL2V2-MMPs-Rα as cis-form after binding to TIM3high T cells, ensuring the need of targeted delivery to TIM3-expressing TILs. Surprisingly, released IL2V2 from TIM3-Rα-MMPs-IL2V2 proved superior in anti-tumor immunity, but not cis delivery form TIM3-IL2V2-MMPs-Rα. Mechanistically, TIM3-ProIL2V2 not only reactivated TIM3+ TILs but also facilitated the activation and expansion of TIM3- T cells which in turn supported a sustained source of TIM3+ effector. TIM3-ProIL2V2 could control multiple tumor models including human tumor in humanized mice, confirming the hypothesis. TIM3-ProIL2V2 activates and expands TIM3-CD8+ T cells to overcome current major unmet medical need: anti-PD-1/L1 resistance. This strategy illustrates the potential of a tailored, low pH-resistant IL2 variant in invigorating both TIM3-negative and positive CD8+ T cells, offering a promising avenue for treating resistant tumors with reduced toxicity.

2025-05-22 | GSE296919 | GEO

Gene expression profile at single cell level of human TILs treated with PD1-TIM3, PD1-LAG3, anti-PD1 or control isotype.

Project description:Several next-generation cancer immunotherapies are designed to target LAG3 and TIM3 checkpoints, though the molecular and cellular mechanisms by which both receptors operate to mediate their anti-tumour effects are still poorly understood. Here, we examined the phenotypical and transcriptional consequences of treatment with bispecific antibodies (bsAbs), currently being tested in clinical trials, which co-target PD1 and either TIM3 or LAG3, respectively, using scRNAseq.

2022-07-16 | GSE208113 | GEO

In vivo study of the Tim3-loss in breast cancer cells during metastasis

Project description:In metastasis, the existence tumor cells overcoming the immune system during early organ seeding is crucial, yet the dynamics of tumor-immune interactions during micrometastasis remain unclear. Examining the immune selective pressure in breast cancer (BC) mouse models, we unexpectedly found TIM3 among the most upregulated genes in metastatic surviving BC cells. The selection of TIM3+ tumor cells, was specifically occurring during early seeding of micrometastasis, escaping the immune attack and acquiring stemness. Also clinical data confirmed increased TIM3+ tumor cells in BC metastasis. The aim of the study was to understand the mechanistic insgihts of Tim3 in breast cancer cells in vivo to decipher pivotal pathways of Tim3-mediated immun-evasion.

2025-07-02 | GSE260480 | GEO

Tumor-activating IL2 rejuvenates intratumoral TIM3-CD8+T cell responses through targeting TIM3+CD8+T cell

Project description:Tumor-activating IL2 rejuvenates intratumoral TIM3-CD8+T cell responses through targeting TIM3+CD8+T cell

| PRJNA1261927 | ENA

Human T-cell dysfunction induced in repeatedly stimulated cultures.

Project description:We report the changes in mRNA profile of quiescent, activated and dysfunctional human CD8+ T cells in culture according to a protocol of weekly polyclonal stimulations relevant to immunotherapy.

2021-08-31 | GSE132727 | GEO

Gene exprsesion profile at single cell level of CD45+ immune cells from 4TO7 cells (Ctrl or Tim3-KD) liver metastasis at different timepoints

Project description:In this study we describe the immunosupressive role of Tim3+ tumor cells during eraly stages of metastasis. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of immune cells subsets altered by Tim3 expression in the tumor cells. The aim was to determine the immune status of immunosuppressive and cytotoxic populations during the dynamic process of the metastatic colonization in the liver

2025-07-02 | GSE260482 | GEO

TNFR2 loss prevents TOX upregulation in CD8+TIM3+ T cells and affords improved responses to tumor and chronic LCMV

Project description:Preview PDF Abstract Exhaustion represents a collection of programmed T cell differentiation states and an important mode of T cell dysfunction. T cell progression from progenitor to terminal exhaustion is associated with upregulation of the transcription factor TOX and expression of TIM3. Our understanding of factors regulating TOX expression and the transition from progenitor to terminal exhaustion, however, remains incomplete. We reveal here that T cell upregulation of tumor necrosis factor receptor type II (TNFR2) coincides with the gain of phenotypic markers and functions reflective of terminal exhaustion. Meanwhile, knocking out TNFR2 affords a novel population of T cells that express TIM3 but possess diminished TOX levels and functional characteristics of both progenitor and terminally exhausted cells. TIM3+ TNFR2 KO T cells exhibit reduced exhaustion transcriptional programs and enhanced AP1 pathway signatures. Finally, TNFR2 KO mice demonstrate improved T cell-dependent control of tumor and chronic lymphocytic choriomeningitis viral (cLCMV) infection, while pharmacologic antagonism of TNFR2 licenses responses to checkpoint blockade in multiple tumor models.

2025-05-19 | GSE297330 | 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