Role of Tim-3 on tumoral Treg cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA591030 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10511937_1.fastq.gz | Fastqsanger.gz | |||
| SRR10511937_2.fastq.gz | Fastqsanger.gz | |||
| SRR10511938_1.fastq.gz | Fastqsanger.gz | |||
| SRR10511938_2.fastq.gz | Fastqsanger.gz | |||
| SRR10511939_1.fastq.gz | Fastqsanger.gz |
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Project description:A gene profiling study revealed the requirement of Tim-3 in upregulation of effector Treg genes encoding immune inhibitory molecules, chemokine receptors for tissue residency, chemokines, and cytokines.
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Project description:TIM-3 is known to be expressed on dendritic cells, monocytes, melanoma cells, mast cells and on activated Th1 cells. In activated Th1 cells, stimulating TIM-3 by one of its ligands, galectin-9, leads to apoptosis and thus it plays a central role in terminating Th1-type immune responses. Interestingly, in IgE/antigen-activated mast cells TIM-3 enhances the production of IL-13 and IL-4. To get a more complete picture about the gene expression changes induced by TIM-3 in mast cells, in vitro differentiated mouse immature mast cells were stimulated by an agonist anti-TIM-3 antibody and IgE-sensitized mouse immature mast cells were activated by antigen and an agonist anti-TIM-3 antibody for 2 or 16 hours (overnight). Experiment Overall Design: Bone marrow cells were differentiated in RPMI + 10% FCS + 5 ng/ml mouse IL-3 + 40 ng/ml mouse SCF for >4 weeks. The purity of the cell cultures was >90% at this time point (FcERIa+/c-kit+ cells). These in vitro-differentiated immature mast cells were then treated by either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml for 2 or 16 hours). For the IgE/antigen-activated mouse mast cells, these in vitro-differentiated immature mast cells were sensitized by 5 ug/ml anti-DNP IgE (Sigma) for 1 hour and then treated with 100 ng/ml DNP-HSA (antigen, Sigma) and either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml) for 2 or 16 hours. The anti-TIM-3 samples were labeled by Cy5 and they were compared to the Cy3-labeled, goat IgG controls in a dual-color, paired experimental setup. The Agilent Whole Mouse Genome 4x44K expression microarray kit and Dual-Color Protocol version 5.5 were used in the experiments.
2009-10-15 | E-GEOD-14438 | biostudies-arrayexpress
Project description:Exhaustion markers are expressed by T lymphocytes in Follicular Lymphoma (FL). Through these, TIM-3 has been recently identified as a poor pronostic factor when expressed by FL CD4+ T cells. Before this study, there was no molecular characterization of unstimulated CD8+ T cells, expressing - or not - TIM-3. We used microarrays to compare the global gene expression profile between CD8+TIM-3+ T cells and CD8+TIM-3- T cells freshly sorted from follicular lymphoma biopsies. Abstract from the associated publication: Up-regulation of T-cell immunoglobulin-3 (TIM-3) has been associated with negative regulation of the immune response in chronic infection and cancer, including lymphoma. Here, we investigated the possible correlation between TIM-3 expression by ex vivo cytotoxic T cells (CTL) from follicular lymphoma (FL) biopsies and their functional unresponsiveness that could limit the favorable impact of CTL on disease progression. We report a high percentage of CD8+TIM-3+ T cells in lymph nodes of FL patients. When compared to their CD8+TIM-3- counterparts, CD8+TIM-3+ T cells exhibited defective cytokine production following TCR engagement. Furthermore CD8+TIM-3+ T cells display ex vivo markers of lytic granule release and remain unresponsive to further TCR-induced activation of the lytic machinery. Although confocal microscopy showed that TIM-3 expression on CD8+ T cells correlated with minor alterations of immunological synapse, a selective reduction of ERK signaling in CD8+TIM-3+ T cells was observed by phospho-flow analysis. Finally, short relapse free survival despite rituximab(R)-chemotherapy was observed in patients with high content of TIM-3+ cells and a poor infiltrate of granzyme B+ T cells in FL lymph nodes. Together, our data indicate that, besides selective TCR early signaling defects, TIM-3 expression correlates with unresponsiveness of ex vivo CD8+ T cells in FL. They show that scores based on the combination of exhaustion and cytolytic markers in FL microenvironment might be instrumental to identify patients at early risk of relapses following R-chemotherapy.
2016-12-15 | GSE84072 | GEO
Project description:Significant differences were found in transcriptional profiles of WT and TIM-3+(GFPHi and GFP Low) cells, suggesting major shifts in metabolic status, cytokine profiles and suppresive capacity of Tregulatory cells due to expression of TIM-3 in Tregulatory cells.
2021-08-16 | GSE155825 | GEO
Project description:The inflammasome initiates innate defense and inflammatory response by activating caspase-1 and pyroptotic cell death in myeloid cells1,2. It is comprised of an innate immune receptor/effector, pro-caspase-1 and a common adaptor molecule, ASC (apoptotic speck-containing protein with a CARD). Consistent with their pro-inflammatory function, inflammasome components including caspase-1, ASC and NLRP3, are known to exacerbate autoimmunity during experimental autoimmune encephalomyelitis (EAE) by enhancing IL-1 and IL-18 secretion in myeloid cells3-6. Here we show an unexpected function of a DNA-binding inflammasome effector, AIM2 (Absent in Melanoma 2)7-10, in restraining autoimmunity by performing EAE in both whole body and Treg-specific deletion of Aim2–/– mice. AIM2 is highly expressed by human and mouse Treg cells and it is essential to attenuate EAE. RNA-seq, biochemical and metabolic analyses revealed that AIM2 attenuates mTOR, Myc and immune-metabolic functions in both Treg cells isolated in vivo and Treg cells induced in vitro with TGF-. Importantly, we found AIM2 physically interacted with RACK1 in Treg cells to facility the PP2A/RACK1/Akt-mTOR signaling, which is identified as a central component downstream of AIM2 that controls Treg cell function and stability. While AIM2 is generally accepted as an inflammasome effector in myeloid cells, this report reveals a previously unappreciated T cell-intrinsic role of AIM2 in maintaining Treg cell function to restrain autoimmunity. This is achieved by diminishing Akt-mTOR signaling to regulate Treg stability under inflammation, and altering immune-metabolism in Treg cells.
2021-01-27 | PXD018638 | Pride
Project description:The goal of this study was to compare the transcriptional profile between different subpopulations of CD8+ T cells in the trigeminal ganglion 8 days post HSV-1 infection. Within the HSV-1 infected TG, essentially all of the CD8+ T cells are virus specific and by using a tetramer for the immunodominant epitope from glycoprotein B (gB), we can separate the CD8+ T cell response into two populations: the gB-CD8+ T cells and the Subdom-CD8+ T cells. These populations have different levels of functionality during viral latency and express different checkpoint molecules that may influence this. Past work has shown that expression of PD-1 is associated with impaired functionality in this model and we are currently investigating the role of Tim-3, as there is little overlap in expression between Tim-3 and PD-1 and Tim-3 appears to mark functional cells when assessed by flow cytometry. By sorting cells first by using tetramer to create two populations of CD8+ T cells and then further separating these populations using expression of Tim-3 and PD-1, we have isolated subpopulations to assess what genes are up and downregulated in Tim-3+ cells compared to Tim-3- cells in each population.
2019-09-26 | GSE137973 | GEO
Project description:RAW264.7 cell was stably transfected with Tim-3 siRNA(SI) or negative control(NC) and were analyzed for microRNA expression Differerently expressed microRNA in Tim-3 knockdown RAW264.7 cells were summarized and were used for further analysis RAW264.7 cells stably transfected with Tim-3 siRNA(SI) or negative control(NC) and were used to collect microRNA without any other treatment
2016-01-14 | E-GEOD-76839 | biostudies-arrayexpress
Project description:Tim-1, a phosphatidylserine receptor expressed on B cells induces IL-10 production by sensing apoptotic cells. Here we show that mice with B cell-specific Tim-1 deletion developed tissue inflammation in multiple organs including spontaneous paralysis with inflammation in the central nervous system (CNS). Transcriptomic analysis demonstrated that besides IL-10, Tim-1+ B cells also differentially expressed a number of co-inhibitory “checkpoint” receptors including TIGIT. Mice with B cell-specific TIGIT deletion developed spontaneous paralysis with CNS inflammation but with limited inflammation in other organs. Our findings suggest that Tim-1+ B cells are essential for maintaining self-tolerance and restraining tissue inflammation, and that Tim-1 dependent TIGIT expression on B cells is essential for maintaining CNS-specific tolerance. A possible critical role of AhR in regulating the B cell function is discussed, as we found that AhR is a top-ranked transcription factor expressed in Tim-1+ B cells and regulates their TIGIT and IL-10 expression.
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Project description:<p>PD-1 is an important immune checkpoint inhibitor that shows great promise in the clinic, particularly for melanoma and lung cancers. Since PD-1 is also expressed on infiltrating CD4+ Treg and Teffector cells in glioblastoma, we sought to better understand the role of PD-1 on these infiltrating CD4+ Treg and Teffector cells. To this end, we performed functional and transcriptional profiling using CD4+ Treg and Teffector cells isolated from healthy donors and glioblastoma patients (from both tumors and blood).</p>
| phs001079 | dbGaP