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Neuropilin-1(NRP1) is a T cell memory checkpoint limiting long-term anti-tumor immunity

ABSTRACT: Neuropilin-1(NRP1) is a T cell memory checkpoint limiting long-term anti-tumor immunity

PROVIDER: PRJNA635953 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11879400.fastq.gz	Fastqsanger.gz
	SRR11879401.fastq.gz	Fastqsanger.gz
	SRR11879402.fastq.gz	Fastqsanger.gz
	SRR11879403.fastq.gz	Fastqsanger.gz
	SRR11879404.fastq.gz	Fastqsanger.gz

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Similar Datasets

Neuropilin-1(NRP1) is a T cell memory checkpoint limiting long-term anti-tumor immunity

Project description:Transcriptomic analysis of NRP1 KO and WT donor pMel-T cells recovered from B16-gp100 tumors

2020-07-01 | GSE151494 | GEO

RNAseq of HUVECs transfected with siRNA targeting Neuropilin 1 (NRP1) (si-NRP1) or a control non-targeting sequence (si-control) and exposed to unidirectional shear stress (20dyns/cm2), oscillatory flow (5dyn/cm2) or kept in absence of flow

Project description:HUVECs transfected with siRNA targeting Neuropilin 1(NRP1) (si-NRP1) or a control non-targeting sequence (si-control) and exposed to unidirectional shear stress (20dyns/cm2), oscillatory flow (5dyn/cm2) or kept in absence of flow.

2023-05-23 | E-MTAB-12191 | biostudies-arrayexpress

Neuropilin-1 is a T cell memory checkpoint limiting long-term antitumor immunity.

Project description:Robust CD8+ T cell memory is essential for long-term protective immunity but is often compromised in cancer, where T cell exhaustion leads to loss of memory precursors. Immunotherapy via checkpoint blockade may not effectively reverse this defect, potentially underlying disease relapse. Here we report that mice with a CD8+ T cell-restricted neuropilin-1 (NRP1) deletion exhibited substantially enhanced protection from tumor rechallenge and sensitivity to anti-PD1 immunotherapy, despite unchanged primary tumor growth. Mechanistically, NRP1 cell-intrinsically limited the self-renewal of the CD44+PD1+TCF1+TIM3- progenitor exhausted T cells, which was associated with their reduced ability to induce c-Jun/AP-1 expression on T cell receptor restimulation, a mechanism that may contribute to terminal T cell exhaustion at the cost of memory differentiation in wild-type tumor-bearing hosts. These data indicate that blockade of NRP1, a unique 'immune memory checkpoint', may promote the development of long-lived tumor-specific Tmem that are essential for durable antitumor immunity.

| S-EPMC7442600 | biostudies-literature

Treg insufficiency in autoimmune diabetes is driven by selective loss of Neuropilin-1 on intra-islet regulatory T cells

Project description:Strategies targeting Treg insufficiency are vital for treating autoimmune diseases like T1D. Our findings highlight the critical role of Neuropilin 1 (Nrp1) in stabilizing Tregs within pancreatic islets. Boosting Nrp1 levels delays diabetes onset by enhancing Treg function. This underscores Nrp1 as a potential target for bolstering Treg activity and combating autoimmune diseases.

2024-08-10 | GSE262874 | GEO

Dnmt3a1 regulates memory formation via the downstram target Nrp1

Project description:Epigenetic factors are well established players in memory formation. Specifically, DNA methylation is necessary for the formation of long-term memory in multiple brain regions including the hippocampus. Despite the demonstrated role for DNA methyltransferases (Dnmts) in memory formation whether individual Dnmts play unique or redundant functions in long-term memory formation is not well established. Furthermore, the downstream processes controlled by the Dnmts during the consolidation of memory are not investigated. In this study, we investigated the requirement for Dnmt3a1, the predominant Dnmt in the adult brain, in hippocampal long-term memory formation. Furthermore, we identified an activity-regulated Dnmt3a1-dependent genomic program. Our data showed that Dnmt3a1, similarly to its isoform Dnmt3a2, plays a critical role in memory formation. Furthermore, we uncovered Neuropilin 1 (Nrp1) as a downstream target of Dnmt3a1 during the formation of memory. Intriguingly, we found that Nrp1 expression is selectively regulated and a specific downstream effector of Dnmt3a1, but not Dnmt3a2. Taken together, our study uncovered a Dnmt3a isoform specific mechanism in memory formation and further highlighted the complex and highly regulated functions of distinct epigenetic regulators in brain function.

2024-05-06 | GSE232630 | GEO

Nrp1 downregulation correlates with enhanced ILC2 responses during IL-33 challenge

Project description:Group 2 innate lymphoid cells (ILC2s) play critical roles in driving the pathogenesis of allergic airway inflammation. The mechanisms underlying the regulation of ILC2s remain to be fully understood. Here, we identified neuropilin-1 (Nrp1) as a surface marker of ILC2s in response to IL-33 stimulation. Nrp1 was abundantly expressed in ILC2s from lung under steady state, which was significantly reduced upon IL-33 stimulation. ILC2s with high expression of Nrp1 (Nrp1high) displayed lower response to IL-33, as compared with Nrp1low ILC2s. Transcriptional profiling and flow cytometric analysis showed that downregulation of AKT-mTOR signaling participated in the diminished functionality of Nrp1high ILC2s. These observations revealed a potential role of Nrp1 in ILC2s responses under allergic inflammatory condition.

2023-09-30 | GSE243540 | GEO

Neuropilin-1 high monocytes protect against neonatal inflammation

Project description:Neonates are susceptible to inflammatory disorders such as necrotizing enterocolitis (NEC) due to their immature immune system. The timely appearance of regulatory immune cells in early life contributes to the control of inflammation in neonates, the underlying mechanisms of which remain poorly understood. In this study, we identified a subset of neonatal monocytes characterized with high levels of neuropilin-1 (Nrp1), termed Nrp1 high monocytes. Nrp1high monocytes displayed potent immunosuppressive activity as compared with their Nrp1low counterpart. Nrp1 deficiency in myeloid cells aggravated the severity of NEC, whereas adoptive transfer of Nrp1 highmonocytes led to remission of NEC. Mechanistic studies showed that Nrp1, via binding to its ligand Sema4a, induced intracellular p38-MAPK/mTOR signaling and activated the transcription factor KLF4. KLF4 transactivated Nos2 and enhanced the production of nitric oxide (NO), a key mediator of immunosuppression in monocytes. These observations uncover an important immunosuppressive axis in neonatal monocytes and provide a potential therapeutic strategy for inflammatory disorders in neonates.

2024-04-12 | GSE263510 | GEO

Neuropilin 1 interactome in endothelial cells

Project description:To get unbiased insights on the molecular networks through by which Neuropilin 1 (NRP1) controls endothelial cell (EC) and blood vessel functions independently from its ligands, wehave implemented a Halo Tag (HT)-based approach, which enables effective surface labeling and pull-down of proteins, and combined it with quantitative mass spectrometry (MS) analysis.

2022-06-15 | PXD019700 | Pride

Neuropilin-1 is Required for the Suppressive Function of Human Regulatory T Cells

Project description:Regulatory T cells (Tregs), lymphocytes that suppress immunological reactions, are of great interest for our comprehension of homeostasis and regulation in the immune system and as a therapeutic target in the treatment of both immune-mediated pathologies and reactivation of the immune response in patients with cancer. Understanding the molecular mechanisms by which these cells are regulated in respone to their environment will help to inform clinical strategies targeting Tregs. We hypothesised that Neuropilin-1, a transmembrane co-receptor for ligands of the semaphorin and growth factor families, promotes the suppressive function of human Tregs. Utilising in vitro lentivirus-mediated transduction with shRNA to knock down neuropilin-1 in primary human Tregs, we demonstrated that neuropilin-1 knockdown Tregs were severely impaired in their capacity to suppress cell proliferation in vitro and in their ability to prolong allograft survival in a humanised mouse model of transplantation. While neuropilin-1-KD Tregs exhibited no defects in survival, proliferation and activation upon stimulation in vitro, we hypothesised that loss of NRP1 expression would alter the global gene expression profile of human Tregs, revealing a NRP1-dependent Treg-associated transcriptional signature.

2019-01-01 | GSE106932 | GEO

Neuropilin-1 mediates lung tissue-specific control of ILC2s function in type 2 immunity

Project description:ILC2s are highly heterogeneous tissue-resident lymphocytes that regulate inflammation and tissue homeostasis in health and disease. But how they integrate to the respective tissue microenvironment to perform tissue-supportive functions remain poorly defined. Here, we identify neuropilin-1, which is induced postnatally and sustained by lung-derived TGFβ1, as a tissue signature of lung ILC2s. Genetic ablation or pharmacological inhibition of Nrp1 suppresses ILC2s function and protects mice from the development of pulmonary fibrosis. Mechanistically, TGFβ1-Nrp1 signaling enhances ILC2s function and type 2 immunity through upregulation of IL-33 receptor ST2 expression. Our findings identify Nrp1 as a tissue-specific regulator of lung-resident ILC2s activation and highlight Nrp1 as a potential therapeutic target for pulmonary fibrosis

2021-10-22 | GSE168809 | GEO

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