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The effects of sorafenib treatment on the T helper cell (Th9) population

ABSTRACT: The effects of sorafenib treatment on the T helper cell (Th9) population

PROVIDER: PRJNA1181543 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31208692_1.fastq.gz	Fastqsanger.gz
	SRR31208692_2.fastq.gz	Fastqsanger.gz
	SRR31208693_1.fastq.gz	Fastqsanger.gz
	SRR31208693_2.fastq.gz	Fastqsanger.gz
	SRR31208694_1.fastq.gz	Fastqsanger.gz

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The effects of sorafenib treatment on the T helper cell (Th9) population

Project description:To investigate the impact of sorafenib treatment on gene expression in Th9 cells, we performed RNA sequencing on Th9 cells treated with sorafenib and on control Th9 cells that were not treated with sorafenib. Here, we found that the up regulation of genes about Il-9.

2025-05-14 | GSE280958 | GEO

The effects of sorafenib treatment on the CD4+T cell population

Project description:To investigate the impact of sorafenib treatment on gene expression in CD4+T cells, we performed RNA sequencing on CD4+T cells treated with sorafenib and on control CD4+T cells that were not treated with sorafenib. Specifically, our study focused on the expression of immune related genes, and we observed an downregulation in the expression of TCR genes.

2025-05-14 | GSE280959 | GEO

The effects of sorafenib treatment on the regulatory T cell (Treg) population

Project description:To investigate the impact of sorafenib treatment on gene expression in Treg cells, we performed RNA sequencing on Treg cells treated with sorafenib and on control Treg cells that were not treated with sorafenib. Specifically, our study focused on the expression of immune-suppressive related genes, and we observed an upregulation in the expression of Tgf-β1 (Transforming Growth Factor-β1), Prf1 (Perforin 1), Gzma (Granzyme A), and Il10 (Interleukin 10).

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The transcription factor BATF3 regulates the differentiation of TH9 cells and TH9-driven mucosal pathologies

Project description:T helper 9 (TH9) cells are important for the development of inflammatory and allergic diseases. The TH9 transcriptional network converge signals from cytokines and antigen presentation but is incompletely understood. Here, we identified TL1A, a member of the TNF superfamily, as strong inducer of mouse and human TH9 differentiation. Mechanistically, TL1A induced the expression of the transcription factors BATF and BATF3 and facilitated their binding to the Il9 promoter leading to enhanced secretion of IL-9. BATF- and BATF3-deficiencies impaired IL-9 secretion under TH9 and TH9-TL1A polarizing conditions. In vivo, using a T cell transfer model we demonstrated that TL1A promoted IL-9-dependent, TH9 cell-induced intestinal and lung inflammation. Neutralizing IL-9 antibodies attenuated TL1A-driven mucosal inflammation. Batf3-/- TH9-TL1A cells induced reduced inflammation and cytokine expression in vivo compared to WT cells. Our results demonstrate that TL1A promotes TH9 cell differentiation and function and define a role of BATF3 in TH9-induced mucosal inflammation.

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The effects of sorafenib treatment on the CD4+T cell population

Project description:The effects of sorafenib treatment on the CD4+T cell population

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The effects of sorafenib treatment on the regulatory T cell (Treg) population

Project description:The effects of sorafenib treatment on the regulatory T cell (Treg) population

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The role of fatty acid metabolism on Th9 cells differentiation

Project description:T helper 9 cells (Th9) are interleukin 9 (IL-9)–producing cells that have diverse functions ranging from anti-tumor immune responses to driving allergic inflammation. Th9 cells differentiate from naïve CD4+ T cells in the presence of IL-4 and transforming growth factor-beta (TGF-β). In this reports, we have found that suppression of fatty acid biosynthesis increased IL-9 production in murine and human Th9 cells. This dataset include a set of data showing the effects of suppression of fatty acid synthesis on gene expression, chromatin remodelling and histone modifications in Th9 cells as analyzed by RNA-seq, ATAC-seq and ChIP-seq, respectively.

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Defining a Th9 transcriptome

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The effects of sorafenib treatment on the Hep1-6 tumor tissue

Project description:This study aimed to investigate the transcriptomic changes in subcutaneous Hepa1-6 tumor tissues of mice following intraperitoneal administration of sorafenib, a tyrosine kinase inhibitor, versus a control solvent. Mice were injected with either sorafenib or the control solvent four times, according to the experimental design. After the treatment period, tumor samples were collected and subjected to RNA sequencing (RNA-seq) to analyze the gene expression profiles. The results from this RNA-seq analysis provide insights into the molecular mechanisms underlying the response of Hepa1-6 tumors to sorafenib treatment, potentially identifying novel therapeutic targets and biomarkers for hepatocellular carcinoma.

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TL1A signaling enhances the differentiation of TH9 cells and TH9-driven mucosal pathologies via BATF and BATF3 signaling pathways

Project description:The TNF family member TL1A (TNFSF15) co-stimulates several T helper subsets and promotes T cell-dependent models of inflammatory diseases, including inflammatory bowel diseases (IBD) and allergic lung disease. TL1A polymorphisms confer susceptibility to IBD and have been associated with disease severity. In this study, we identified TL1A as a strong inducer of TH9 cell differentiation in vitro. Mechanistically, TL1A induced NF-B signaling and down-stream STAT6 activation and facilitated cooperative binding of BATF, BATF3, and IRF4 to the Il9 promoter. In vivo, utilizing an adoptive T cell transfer model we demonstrated that TL1A promoted IL-9-dependent, TH9 cell-induced intestinal and lung inflammation and blocking anti-IL-9 antibodies attenuated TL1A-driven mucosal inflammation. Our results demonstrate that TL1A promotes TH9 cell differentiation and function and define a role for IL-9 in TL1A-induced mucosal inflammation.

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