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TIM-3 restrains anti-tumour immunity by regulating inflammasome activation.

ABSTRACT: TIM-3 restrains anti-tumour immunity by regulating inflammasome activation.

PROVIDER: PRJNA637635 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11937745.fastq.gz	Fastqsanger.gz
	SRR11937746.fastq.gz	Fastqsanger.gz

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TIM-3 restrains anti-tumour immunity by regulating inflammasome activation.

Project description:Droplet-based massively parallel single-cell RNA sequencing (scRNAseq) was performed by encapsulating sorted live CD45+ tumour-infiltrating cells into droplets and libraries were prepared using Chromium Single Cell 5′ Reagent Kits v2 according to the manufacturer’s protocol (10X Genomics). The generated scRNA-seq libraries were sequenced using an Illumina HiSeq2500.

2021-06-08 | GSE151914 | GEO

TIM-3 restrains anti-tumour immunity by regulating inflammasome activation.

Project description:T cell immunoglobulin and mucin-containing molecule 3 (TIM-3), first identified as a molecule expressed on interferon-γ producing T cells1, is emerging as an important immune-checkpoint molecule, with therapeutic blockade of TIM-3 being investigated in multiple human malignancies. Expression of TIM-3 on CD8+ T cells in the tumour microenvironment is considered a cardinal sign of T cell dysfunction; however, TIM-3 is also expressed on several other types of immune cell, confounding interpretation of results following blockade using anti-TIM-3 monoclonal antibodies. Here, using conditional knockouts of TIM-3 together with single-cell RNA sequencing, we demonstrate the singular importance of TIM-3 on dendritic cells (DCs), whereby loss of TIM-3 on DCs-but not on CD4+ or CD8+ T cells-promotes strong anti-tumour immunity. Loss of TIM-3 prevented DCs from expressing a regulatory program and facilitated the maintenance of CD8+ effector and stem-like T cells. Conditional deletion of TIM-3 in DCs led to increased accumulation of reactive oxygen species resulting in NLRP3 inflammasome activation. Inhibition of inflammasome activation, or downstream effector cytokines interleukin-1β (IL-1β) and IL-18, completely abrogated the protective anti-tumour immunity observed with TIM-3 deletion in DCs. Together, our findings reveal an important role for TIM-3 in regulating DC function and underscore the potential of TIM-3 blockade in promoting anti-tumour immunity by regulating inflammasome activation.

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Oxidized thioredoxin-1 restrains the NLRP1 inflammasome.

Project description:Oxidized thioredoxin-1 restrains the NLRP1 inflammasome.

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Oxidized thioredoxin-1 restrains the NLRP1 inflammasome [mBMDM]

Project description:Oxidized thioredoxin-1 restrains the NLRP1 inflammasome [mBMDM]

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Oxidized thioredoxin-1 restrains the NLRP1 inflammasome [NTERT-1]

Project description:Oxidized thioredoxin-1 restrains the NLRP1 inflammasome [NTERT-1]

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Ptpn2 regulates the generation of cytotoxic Tim-3+ CD8+ T cells and restrains anti-tumor immunity

Project description:Ptpn2 regulates the generation of cytotoxic Tim-3+ CD8+ T cells and restrains anti-tumor immunity

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Tim-3 Agonist Restrains ILC2 Function and Attenuates Airway Hyperreactivity via NLK Pathway

Project description:Allergic asthma is driven by type 2 inflammation involving cytokines such as IL-4, IL-5, and IL-13, with group 2 innate lymphoid cells (ILC2s) playing a key pathogenic role. Here, we identify T cell immunoglobulin and mucin domain-containing protein 3 (Tim-3) as a negative regulator of ILC2 function. Tim-3 expression was upregulated in activated pulmonary ILC2s, and engagement with Tim-3 agonists inhibited ILC2 activation, proliferation, and type 2 cytokine production via the NLK signaling pathway and suppression of mitochondrial metabolism. In vivo, Tim-3 agonists alleviated airway hyperreactivity (AHR) and inflammation in both IL-33- and Alternaria alternata-induced AHR models, while ILC2-specific Tim-3 deletion exacerbated AHR. These results were confirmed in human ILC2s and humanized mice, supporting the translational relevance. Our findings establish Tim-3 as an inhibitory checkpoint for ILC2s and suggest its potential as a therapeutic target in allergic asthma and other ILC2-mediated diseases.

2026-02-22 | GSE298909 | GEO

Tim-3 Agonist Restrains ILC2 Function and Attenuates Airway Hyperreactivity via NLK Pathway

Project description:Tim-3 Agonist Restrains ILC2 Function and Attenuates Airway Hyperreactivity via NLK Pathway

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Oxidized thioredoxin-1 restrains the NLRP1 inflammasome [mBMDM]

Project description:The danger signals that activate the NLRP1 inflammasome have yet to be firmly established. NLRP1 undergoes autoproteolysis to generate N-terminal (NT) and C-terminal (CT) fragment, which importantly, is a necessary step for its check-point regulation by the DPP9 ternary complex and the mechanistic activation of NLRP1 through functional degradation. Here, we report an added layer of regulatory complexity to NLRP1 activity, in the form of a repressive interaction that NLRP1 forms with the oxidized, but not reduced, form of thioredoxin-1 (TRX1). Loss of TRX1 destabilizes the NT fragment of NLRP1 and promotes enhanced inflammasome activation. The TRX1 interaction occurs through the NACHT-LRR of NLRP1 and requires nucleotide binding in its ATPase domain. In addition, we found that several patient-derived and ATPase-inactivating mutations in the NACHT-LRR region hyperactive the inflammasome by destabilize protein folding and are also shown to abrogate TRX1 binding. Thus, NLRP1 appears to detect intracellular reductive stress through a decrease in the fraction of intracellular oxidized TRX1, which enhances protein disorder, leading to inflammasome signaling. These findings link the cellular redox environment to NLRP1-mediated innate immunity.

2022-11-04 | GSE215035 | GEO

Oxidized thioredoxin-1 restrains the NLRP1 inflammasome [NTERT-1]

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