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Lipid droplets impair anti-tumor immunity by disrupting IFNGR1 trafficking via TGN diacylglycerol depletion

ABSTRACT: Lipid droplets impair anti-tumor immunity by disrupting IFNGR1 trafficking via TGN diacylglycerol depletion

PROVIDER: PRJNA1225122 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32377653_1.fastq.gz	Fastqsanger.gz
	SRR32377653_2.fastq.gz	Fastqsanger.gz
	SRR32377654_1.fastq.gz	Fastqsanger.gz
	SRR32377654_2.fastq.gz	Fastqsanger.gz
	SRR32377655_1.fastq.gz	Fastqsanger.gz

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Lipid droplets impair anti-tumor immunity by disrupting IFNGR1 trafficking via TGN diacylglycerol depletion

Project description:Lipid droplets (LDs) are dynamic organelles that regulate cellular metabolism, yet their role in tumor immune evasion remains unclear. Here, we demonstrate that LDs impair anti-tumor immunity by disrupting the membrane localization of interferon-gamma receptor 1 (IFNGR1). Tumor cells with reduced LD content exhibit heightened susceptibility to immune-mediated cytotoxicity in vitro, in murine immunotherapy models, and in patients undergoing immune checkpoint blockade. Mechanistically, IFNGR1 trafficking to the plasma membrane is dependent on diacylglycerol (DAG) in the trans-Golgi network (TGN). However, LDs sequester DAG, impeding IFNGR1 trafficking and attenuating JAK2-STAT1 signaling. Notably, genetic or pharmacological depletion of LDs enhances tumor sensitivity to anti-PD-1 therapy. These findings establish LDs as immunosuppressive organelles that compromise interferon signaling, highlighting their potential as therapeutic targets to improve cancer immunotherapy outcomes.

2025-03-01 | GSE289818 | GEO

Zebrafish are resilient to the loss of major diacylglycerol acyltransferase enzymes

Project description:In zebrafish, maternally deposited yolk is the source of nutrients for embryogenesis prior to digestive system maturation. Yolk nutrients are processed and secreted to the growing organism by an extra-embryonic tissue, the yolk syncytial layer (YSL). Export of lipid from the YSL occurs through the production of triacylglycerol-rich lipoproteins. Here we report that mutations in the triacylglycerol synthesis enzyme, diacylglycerol acyltransferase-2 (Dgat2), cause yolk sac opacity due to aberrant accumulation of cytoplasmic lipid droplets in the YSL. Though triacylglycerol synthesis continues, it is not properly coupled to lipoprotein production as dgat2 mutants produce fewer, smaller, ApoB-containing lipoproteins. Unlike DGAT2-null mice, which are lipopenic and die soon after birth, zebrafish dgat2 mutants are viable, fertile and exhibit normal mass and adiposity. Residual Dgat activity cannot be explained by the activity of other known Dgat isoenzymes, as dgat1a;dgat1b;dgat2 triple mutants continue to produce YSL lipid droplets and remain viable as adults. Further, the newly identified diacylglycerol acyltransferase, Tmem68, is also not responsible for the residual triacylglycerol synthesis activity. Unlike overexpression of Dgat1a and Dgat1b, monoacylglycerol acyltransferase-3 (Mogat3b) overexpression does not rescue yolk opacity, suggesting it does not possess Dgat activity in the YSL. However, mogat3b;dgat2 double mutants exhibit increased yolk opacity and often have structural alterations of the yolk extension. Quadruple mogat3b;dgat1a;dgat1b;dgat2 mutants either have severely reduced viability and stunted growth, or do not survive past 3 days post fertilization, depending on the dgat2 mutant allele present. Our study highlights the remarkable ability of vertebrates to synthesize triacylglycerol through multiple biosynthetic pathways.

2024-11-07 | GSE279170 | GEO

Lipid Droplet–Mediated Depletion of DAG in the TGN Impairs IFNGR1 Membrane Localization and Anti-Tumor Immunity

2025-11-03 | PXD070259 |

Extracellular vesicles from neural stem cells transfer IFN-? via Ifngr1 to activate Stat1 signalling in target cells

Project description:The idea that stem cell therapies work only via cell replacement is challenged by the observation of consistent intercellular molecule exchange between the graft and the host. Here we defined a mechanism of cellular signaling by which neural stem/precursor cells (NPCs) communicate with the microenvironment via extracellular vesicles (EVs), and we elucidated its molecular signature and function. We observed cytokine-regulated pathways that sort proteins and mRNAs into EVs. We described induction of interferon gamma (IFN-?) pathway in NPCs exposed to proinflammatory cytokines that is mirrored in EVs. We showed that IFN-? bound to EVs through Ifngr1 activates Stat1 in target cells. Finally, we demonstrated that endogenous Stat1 and Ifngr1 in target cells are indispensable to sustain the activation of Stat1 signaling by EV-associated IFN-?/Ifngr1 complexes. Our study identifies a mechanism of cellular signaling regulated by EV-associated IFN-?/Ifngr1 complexes, which grafted stem cells may use to communicate with the host immune system. polyA RNA profiling of Neural Stem/Progenitor cells (NPCs) cultured in basal/Th1/Th2 conditions, of Exosomes derived from NPCs cultured in basal/Th1/Th2 conditions and of EVs derived from NPCs cultured in Basal/Th1/Th2 conditions. Total RNA was purified using Trizol. Purity and integrity were confirmed by BioAnalyser (Agilent). Paired End library construction and poly-A selection were performed by EASIH (The Eastern Sequence and Informatics Hub, University of Cambridge, Cambridge) according to the Illumina standard protocol. Sequencing was performed by EASIH using Illumina GAII.

2014-09-22 | E-GEOD-33527 | biostudies-arrayexpress

Transcriptome profiling of phagocytic or non-phagocytic microglia from Ifngr1 cKO mice.

Project description:Investigate the effect of depleting Ifngr1 in microglia on their response to acute neurodegeneration

2023-04-10 | GSE221080 | GEO

Pitch Lake water droplets

Project description:Pitch Lake water droplets Raw sequence reads

| PRJNA1010525 | ENA

Single cell RNA-sequencing of lungs of Ifngr1-/-Rag-2-/- mice

Project description:We discovered Ifngr1-/-Rag-2-/- mice spontaneously develop severe pulmonary fibrosis (PF), and divided the progression process of PF in this strain into 3 phases; the pre-disease phase (until 12 weeks old; intact), the onset phase (from 12 to 18 weeks old; characterized by inflammations), and the chronic phase (after 18 weeks old; characterized by collagen deposition and obvious clinical symptoms). For the purpose of understanding the transcriptome dynamics of each phase, we performed single-cell RNA-Seq analysis on the whole lung cells from Rag-2-/- mice and Ifngr1-/-Rag-2-/- mice of different ages, including the pre-disease (7 weeks old), the onset (12 and 16 weeks old), and chronic phases (19 and 24weeks old).

2023-11-04 | GSE164220 | GEO

Extracellular vesicles from neural stem cells transfer IFN-γ via Ifngr1 to activate Stat1 signalling in target cells

2014-09-22 | GSE33527 | GEO

Protein phosphorylation of IFNgR1 knockout B16 cells

Project description:B16 cells were transduced by lentivirus encoding scramble shRNA and engineered to obtain two IFNgR1-knockout cell clones. Proteins from these cells were digested by TPCK-trypsin. Equal amount of peptides were labelled with TMTpro reagents and pooled. Phosphopeptides were enriched from 90% of the pooled peptides using TiO2 beads, and fractionated with the Pierce high pH reversed-phase peptide fractionation kit to get six fractions. The remaining 10% pooled peptides (called total peptides) were fractionated similarly to get five fractions. Peptides from each fraction were analyzed using HPLC-ESI-MS/MS. Some fractions were analyzed twice. TMTpro channels 1-4: four independent samples of scramble shRNA group; channels 5-8: four independent samples of IFNgR1 knockout cell clone 1; channels 9-12: four independent samples of IFNgR1 knockout cell clone 2; channels 13-16: samples not related to this study.

2021-07-12 | MSV000087796 | MassIVE

In vivo CRISPR screens for Toxoplasma using metabolism sublibrary in WT and Ifngr1-deficient mice

Project description:We performed in vivo CRISPR screen of Toxoplasma targeting metabolism-related genes to identify in vivo fitness genes in WT and Ifngr1-deficient mice.

2023-06-12 | GSE229548 | GEO

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