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PTBP1 is necessary for dendritic cells to regulate T cells homeostasis and antitumor immunity

ABSTRACT: PTBP1 is necessary for dendritic cells to regulate T cells homeostasis and antitumor immunity

PROVIDER: PRJNA642299 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12102210_1.fastq.gz	Fastqsanger.gz
	SRR12102210_2.fastq.gz	Fastqsanger.gz
	SRR12102211_1.fastq.gz	Fastqsanger.gz
	SRR12102211_2.fastq.gz	Fastqsanger.gz
	SRR12102212_1.fastq.gz	Fastqsanger.gz

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PTBP1 is necessary for dendritic cells to regulate T cells homeostasis and antitumor immunity

Project description:Dendritic cells (DCs) play an important role in innate and adaptive immunity. DCs could sense environment pathogens and tumors, presenting those antigens to T cells. PTBP1, an RNA-binding protein, the function in DCs is unknown. Here, we found PTBP1 specific deficiency in DCs could impair T cell homeostasis. PTBP1 deletion in DCs could enhance antitumor immunity and increase asthma exacerbation. Further studies demonstrate that PTBP1 negatively regulates the induction of a subset of IFN-response genes. These findings revealed the novel functions of PTBP1 in DCs and might be a potential therapeutic target for tumors.

2021-01-10 | GSE153401 | GEO

The RNA binding protein PTBP1 is necessary for B cell selection in germinal centres

Project description:Antibody affinity maturation occurs in germinal centres (GC) where B cells cycle between the light zone (LZ) and the dark zone. In the LZ GC B cells bearing immunoglobulins with the highest affinity for antigen receive positive selection signals from T helper cells that promotes their rapid proliferation. Here we show that the RNA binding protein PTBP1 is necessary for the progression of GC B cells through late S-phase of the cell cycle and for affinity maturation. PTBP1 is required for the expression of the c-MYC-dependent gene programme induced in GC B cells receiving T cell help and directly regulates the alternative splicing of transcripts increased during positive selection to promote anabolic metabolism and cell proliferation.

2017-12-06 | GSE100969 | GEO

Targeting WEE1 in tumor-associated dendritic cells potentiates antitumor immunity

Project description:Targeting WEE1 in tumor-associated dendritic cells potentiates antitumor immunity

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Proteome changes in PTBP1 deficient hematopoietic cells

Project description:Ribosomopathies constitute a range of disabling conditions associated with defective protein synthesis mainly affecting hematopoietic stem cells (HSCs) and erythroid development. Here we demonstrate that deletion of Polypyrimidine Tract Binding Protein 1 (PTBP1) in the hematopoietic compartment led to the development of a ribosomopathy-like condition. Specifically, loss of PTBP1 was associated with a decrease in HSC self-renewal, erythroid differentiation and protein synthesis. Consistent with its function as a splicing regulator, PTBP1 deficiency led to splicing defects in hundreds of genes and we demonstrate that the up-regulation of a specific isoform of CDC42 could partly mimic the protein synthesis defect associated with loss of PTBP1. Furthermore, PTBP1 deficiency was associated with a marked defect in ribosome biogenesis and a selective reduction in the translation of mRNAs encoding ribosomal proteins. Collectively, this work identifies PTBP1 as a key integrator of ribosomal functions and highlights the broad functional repertoire of RNA binding proteins.

2022-05-04 | PXD023879 | Pride

PTBP1 is necessary for dendritic cells to regulate T-cell homeostasis and antitumour immunity.

Project description:Dendritic cells (DCs) play an important role in linking innate and adaptive immunity. DCs can sense endogenous and exogenous antigens and present those antigens to T cells to induce an immune response or immune tolerance. During activation, alternative splicing (AS) in DCs is dramatically changed to induce cytokine secretion and upregulation of surface marker expression. PTBP1, an RNA-binding protein, is essential in alternative splicing, but the function of PTBP1 in DCs is unknown. Here, we found that a specific deficiency of Ptbp1 in DCs could increase MHC II expression and perturb T-cell homeostasis without affecting DC development. Functionally, Ptbp1 deletion in DCs could enhance antitumour immunity and asthma exacerbation. Mechanistically, we found that Pkm alternative splicing and a subset of Ifn response genes could be regulated by PTBP1. These findings revealed the function of PTBP1 in DCs and indicated that PTBP1 might be a novel therapeutic target for antitumour treatment.

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Network-based screening identifies sitagliptin as an antitumor drug targeting dendritic cells

Project description:Network-based screening identifies sitagliptin as an antitumor drug targeting dendritic cells

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Targeting WEE1 in tumor-associated dendritic cells potentiates antitumor immunity [scRNA-Seq]

Project description:Targeting WEE1 in tumor-associated dendritic cells potentiates antitumor immunity [scRNA-Seq]

| PRJNA1122520 | ENA

iiCLIP protocol benchmarking with PTBP1

Project description:We describe an improved individual nucleotide resolution CLIP protocol (iiCLIP), which can be completed within 4 days from UV crosslinking to libraries for sequencing. For benchmarking, we directly compared PTBP1 iiCLIP libraries with the iCLIP2 protocol produced under standardised conditions with 1 million HEK293 cells, and with public eCLIP and iCLIP PTBP1 data. There are 3 PTBP1 iiCLIP libraries, 1 input iiCLIP library and 1 PTBP1 iCLIP2 library produced in this study.

2022-08-01 | E-MTAB-10881 | biostudies-arrayexpress

Antitumor therapeutic vaccination induces immunosuppressive dendritic cells

Project description:Vaccination induces immunostimulatory signals which are often accompanied by regulatory mechanisms such as IL-10, which control T-cell activation and inhibit vaccine-dependent antitumor therapeutic effect. Thus, here we characterized IL-10-producing cells treated with therapeutic vaccines. Although several cell subsets produced IL-10 irrespective of treatment, an early vaccine-dependent induction of IL-10 was detected in dendritic cells (DC). IL-10 production defined a DC population characterized by a poorly mature phenotype, lower expression of T-cell stimulating molecules and upregulation of PD-L1. These IL-10+ DC showed impaired in vitro T-cell stimulatory capacity, which was rescued by incubation with IL-10R and PD-L1-inhibiting antibodies. In vivo IL-10 blockade during vaccination decreased the proportion of IL-10+ DC and improved their maturation, without modifying PD-L1 expression. Similarly, PD-L1 blockade did not affect IL-10 expression, suggesting independent regulation of these molecules. Interestingly, vaccination combined with simultaneous blockade of IL-10 and PD-L1 induced stronger immune responses, resulting in a higher therapeutic efficacy in tumor-bearing mice. These results show that vaccine-induced immunoregulatory DC with dual expression of IL-10 and PD-L1 impair priming of antitumor immunity, suggesting that therapeutic vaccination protocols may benefit from combined targeting of these molecules.

2017-06-10 | GSE84980 | GEO

Tumor-Pulsed Dendritic Cells Used as a Tumor Vaccine

Project description:This study is being conducted to determine the efficacy, side effects, and toxicity of an investigational vaccine that consists of tumor-pulsed dendritic cells administered with an immune stimulating drug called interleukin-2 (IL-2). Dendritic cells are immune cells that are obtained from a subject’s blood and are important in the body’s immune response to foreign substances. This study will examine the response of a subject’s immune system after receiving several vaccinations containing their own dendritic cells which have been exposed to dead fragments of their cancer cells in the laboratory. This may result in sensitizing a subject’s dendritic cells to their cancer cells so that their dendritic cells will react with other cells of the immune system and attack the cancer. It has been shown in the laboratory that dendritic cells exposed to cancer cell fragments can provide lymphocytes (a type of white blood cell) with signals they require in order to become fully activated and acquire the ability to kill cancer cells.

| 2017769 | ecrin-mdr-crc

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