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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE260482 | GEO | 2025/07/02

REPOSITORIES: GEO

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			Action	DRS
		Other
	GSE260482_Li-Ma.barcodes.tsv.gz	Tabular
	GSE260482_Li-Ma.features.tsv.gz	Tabular
	GSE260482_Li-Ma.matrix.mtx.gz	Other
	GSE260482_Li-Mi.barcodes.tsv.gz	Tabular

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

| PRJNA1081867 | 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

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

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

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

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

Identification of a T-bet hi Quiescent Exhausted CD8 T Cell Subpopulation That Can Differentiate into TIM3 + CX3CR1 + Effectors and Memory-like Cells

Project description:Persistent Ag induces a dysfunctional CD8 T cell state known as "exhaustion" characterized by PD-1 expression. Nevertheless, exhausted CD8 T cells retain functionality through continued differentiation of progenitor into effector cells. However, it remains ill-defined how CD8 T cell effector responses are sustained in situ. In this study, we show using the mouse chronic lymphocytic choriomeningitis virus infection model that CX3CR1+ CD8 T cells contain a T-bet-dependent TIM3-PD-1lo subpopulation that is distinct from the TIM3+CX3CR1+PD-1+ proliferative effector subset. The TIM3-CX3CR1+ cells are quiescent and express a low but significant level of the transcription factor TCF-1, demonstrating similarity to TCF-1hi progenitor CD8 T cells. Furthermore, following the resolution of lymphocytic choriomeningitis virus viremia, a substantial proportion of TCF-1+ memory-like CD8 T cells show evidence of CX3CR1 expression during the chronic phase of the infection. Our results suggest a subset of the CX3CR1+ exhausted population demonstrates progenitor-like features that support the generation of the CX3CR1+ effector pool from the TCF-1hi progenitors and contribute to the memory-like pool following the resolution of viremia.

2021-04-13 | GSE148497 | 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: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.

2024-08-23 | GSE181682 | GEO

CD45+ and CD45- cells of benign v/s metastatic mouse breast tumors

Project description:Metastasis remains a leading cause of all cancer related mortalities and therapeutic challenges. To successfully establish tumors and metastasiz, cancer cells must escape recognition and elimination by modulating immune cells during surveillance. Therapies that mount anti-tumor response of the adaptive immune system and target the immune evasion mechanisms have entered the clinic. However, the number of patients that respond to these therapies remains humble. This is likely due to the pro-tumor and immunosuppressive mechanisms of innate immune system that remain elusive. Tumor immune cells demonstrate tremendous intra- and inter-tumoral heterogeneity. Presence of high neutrophil to lymphocyte ratio is typically associated with high risk of metastasis and poor patient outcome, which suggests that immune cells, specifically myeloid cells of metastatic tumors have distinct biological functions. We aim to identify these distinct biological functions and the candidates that may have prognostic and therapeutic potential using a non-metastatic and metastatic tumor from the 4T1 mouse breast cancer model.

2023-11-22 | GSE211223 | GEO

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