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50 results for “TIM-3;”
Identification of a small molecule Tim-3 inhibitor to potentiate T cell-mediated antitumor immunotherapy in preclinical models
<p><span>T cell immunoglobulin and mucin-containing molecule 3 (Tim-3), expressed in dysfunctional and exhausted T cells, has been widely acknowledged as a promising immune checkpoint target for tumor immunotherapy. Here, using a strategy combining virtual and functional screening, we identified a compound named ML-T7 that targets the FG-CC' cleft of Tim-3, a highly conserved binding site of </span><span>phosphatidylserine</span><span> (PtdSer) and carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1). ML-T7 enhanced the survival and antitumor activity of </span><span>primary CD8<sup>+</sup> cytotoxic T lymphocytes (CTLs) and human chimeric antigen receptor (CAR) T cells and reduced their exhaustion </span><span>in vitro and in vivo</span><span>. In addition, ML-T7 promoted NK cells' killing activity and DC antigen-presenting capacity, consistent with the reported activity of Tim-3.</span><span> Notably, ML-T7 strengthened DCs' functions through both Tim-3 and Tim-4, consistent with the hypothesis that Tim-4 contains a similar FG-CC' loop. Intraperitoneal dosing of ML-T7 showed comparable tumor inhibitory effects to Tim-3 blocking antibody. ML-T7 reduced syngeneic tumor progression in both wildtype and Tim-3 humanized mice and alleviated the immunosuppressive microenvironment. Furthermore, combined ML-T7 and anti-PD-1 therapy had greater therapeutic efficacy than monotherapy in mice, supporting further development of ML-T7 for tumor immunotherapy. Our study demonstrates a potential small molecule for selectively blocking Tim-3 and warrants further study.</span></p>
Identification of a small molecule Tim-3 inhibitor to potentiate T cell-mediated antitumor immunotherapy in preclinical models
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Tim-3 regulates the immunosuppressive function of decidual MDSCs via the Fyn-STAT3-C/EBPβ pathway during Toxoplasma gondii infection
<p><span>Myeloid-derived suppressor cells (MDSCs) play a key role in maintaining maternal-fetal tolerance for a successful pregnancy, but the role of MDSCs in abnormal pregnancy caused by <em>Toxoplasma</em> <em>gondii</em> infection is unknown. Herein, we revealed a distinct mechanism by which T-cell immunoglobulin domain- and mucin domain-containing protein-3 (Tim-3), an immune checkpoint receptor that balances maternal-fetal tolerance during pregnancy, contributes to the immunosuppressive function of MDSCs during <em>T. gondii</em> infection. The expression of Tim-3 in decidual MDSCs was significantly </span><span>downregulated</span><span> following <em>T. gondii </em>infection. The proportion of monocytic </span><span>MDSC</span><span> population, the inhibitory effect of MDSCs on T-cell proliferation, the levels of STAT3 phosphorylation, and the expression of functional molecules (Arg-1 and IL-10) in MDSCs were all decreased in <em>T. gondii</em>-infected pregnant Tim-3 gene knockout (Tim-3KO) mice compared with infected pregnant WT mice. After treatment with Tim-3-neutralizing Ab <em>in vitro</em>, the expression levels of Arg-1, IL-10, C/EBPβ, and p-STAT3 were decreased, the interaction between Fyn and Tim-3 or between Fyn and STAT3 </span><span>was</span><span> weakened,</span><span> and</span><span> the binding ability of C/EBPβ to the promoters of <em>ARG1</em> and <em>IL10</em> </span><span>was</span><span> decreased in human decidual MDSCs with <em>T. gondii</em> infection, while opposite results were observed following treatment with galectin-9 (a ligand for Tim-3). </span><span>Inhibitors</span><span> of Fyn and STAT3 also </span><span>downregulated</span><span> the expression of Arg-1 and IL-10 in decidual MDSCs and exacerbated adverse pregnancy outcomes caused by <em>T. gondii</em> infection in mice. Therefore, our studies discovered that the decrease of Tim-3 after <em>T. gondii</em> infection could downregulate the functional molecules of Arg-1 and IL-10 expression in decidual MDSCs through the Fyn-STAT3-C/EBPβ signaling pathway and weaken their immunosuppressive function, which eventually contributes to the development of adverse pregnancy outcomes.</span></p>
Dynamic Changes of Tim-3 on Monocytes and Soluble Tim-3 in Patients With Sepsis
ClinicalTrials.gov study NCT02180009. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Neoadjuvant PD-1 Inhibitor Dostarlimab (TSR-042) vs. Combination of Tim-3 Inhibitor Cobolimab (TSR-022) and PD-1 Inhibitor Dostarlimab (TSR-042) in Melanoma
ClinicalTrials.gov study NCT04139902. IPD Sharing: NO. Countries: 1. Publications: 1.
Tim-3 regulates the immunosuppressive function of decidual MDSCs via the Fyn-STAT3-C/EBPβ pathway during Toxoplasma gondii infection
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Immune checkpoint TIM-3 regulates microglia and Alzheimer’s disease
GEO Series GSE223424. Mus musculus. 57 samples. Type: Expression profiling by high throughput sequencing.
Immune checkpoint TIM-3 regulates microglia and Alzheimer’s disease [snRNAseq_5M]
GEO Series GSE223423. Mus musculus. 10 samples. Type: Expression profiling by high throughput sequencing.
Bulk RNA-Seq profiling of progenitor exhausted (Slamf6+Tim-3-) and terminally exhausted (Slamf6-Tim-3+) CD8+ T-cells from tumors and chronic viral infection
GEO Series GSE123235. Mus musculus. 54 samples. Type: Expression profiling by high throughput sequencing.
Next Generation Sequencing of Transcriptomes of WT and Transgenic Treg cells to differentiate effect of TIM-3 on Tregulatory cell geneexpression.
GEO Series GSE155825. Mus musculus. 8 samples. Type: Expression profiling by high throughput sequencing.
targeted single-cell RNA sequencing data of residual TIM-3+ leukemic stem cells post-SCT_2
GEO Series GSE206251. Homo sapiens. 1 samples. Type: Expression profiling by high throughput sequencing.
Effect of TIM-3 knockout in the tumoroginesis in the NP53 DMG cell line
GEO Series GSE223859. Mus musculus. 9 samples. Type: Expression profiling by high throughput sequencing.
TIM-3 restrains anti-tumour immunity by regulating inflammasome activation.
GEO Series GSE151914. Mus musculus. 2 samples. Type: Expression profiling by high throughput sequencing.
beta-catenin in dendritic cells negatively regulates CD8 T cell im-mune responses through the immune checkpoint molecule Tim-3
GEO Series GSE263715. Mus musculus. 2 samples. Type: Expression profiling by high throughput sequencing.
Triple checkpoint blockade of PD-1, Tim-1 3 and Lag-3, but not PD-1 alone, enhances adoptive T cell immunotherapy in a mouse model of ovarian cancer
GEO Series GSE306904. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Ptpn2 regulates the generation of cytotoxic Tim-3+ CD8+ T cells and restrains anti-tumor immunity
GEO Series GSE119270. Mus musculus. 39 samples. Type: Expression profiling by high throughput sequencing.
Epithelial Ovarian Cancer is infiltrated by activated effector T cells co-expressing CD39, PD-1, TIM-3, CD137 and interacting with cancer cells and myeloid cells
GEO Series GSE243751. Homo sapiens. 46 samples. Type: Expression profiling by array.
TIM-3, LAG-3, or 2B4 gene disruptions increase the anti-tumor response of engineered T cells
GEO Series GSE256035. Homo sapiens. 22 samples. Type: Expression profiling by high throughput sequencing.
Immune checkpoint molecule Tim-3 regulates microglial function and the development of Alzheimer’s disease pathology [scRNA-Seq]
GEO Series GSE267764. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
Microarray analysis of the effect of shRNA-mediated HAVCR2 knock-down (KD) in TIM-3-positive AML cell line, KASUMI-3
GEO Series GSE130328. Homo sapiens. 6 samples. Type: Expression profiling by array.
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