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

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

PROVIDER: PRJNA418449 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6293380.fastq.gz	Fastqsanger.gz
	SRR6293381.fastq.gz	Fastqsanger.gz
	SRR6293382.fastq.gz	Fastqsanger.gz
	SRR6293379.fastq.gz	Fastqsanger.gz

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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.

2019-01-08 | GSE106926 | GEO

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.

2019-01-08 | GSE60362 | GEO

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

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Transcriptional modifications driven by STING activation in polarizing TH1 and Th9 cells

Project description:We assessed the global transcriptional changes driven by STING activation with the cyclic dinucleotide 2'3'-cGAMP TH1 and TH9 cells polarized in vitro for 16h and 48h. Our data indicated that STING activation led to an upregulation of Type I Interferon, Interferon Stimulated Genes and pro-inflammatory molecule production that was maintained over time. Furthermore, not only STING activation enhanced the transcription of TH1 and TH9 main effector cytokines (respectively Ifng and Il9) but they also also globally enhanced their differentiation programs.

2022-02-18 | GSE147300 | GEO

A role for BATF3 in T<sub>H</sub>9 differentiation and T-cell-driven mucosal pathologies.

Project description:T helper 9 (TH9) cells are important for the development of inflammatory and allergic diseases. The TH9 transcriptional network converges signals from cytokines and antigen presentation but is incompletely understood. Here, we identified TL1A, a member of the TNF superfamily, as a 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 for BATF3 in T-cell-driven mucosal inflammation.

| S-EPMC6462229 | biostudies-literature

Defining a Th9 transcriptome

Project description:Microarray analyses were performed to compare gene expression in cultured mouse Th9, Th2 and Treg cells and resting versus activated Th9 cells. Three replicates were analyzed for each culture condition; Th9 unstim, Th2 unstim, Treg unstim, Th9 stim

2014-03-26 | E-GEOD-44937 | biostudies-arrayexpress

Defining a Th9 transcriptome

Project description:Microarray analyses were performed to compare gene expression in cultured mouse Th9, Th2 and Treg cells and resting versus activated Th9 cells.

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Transcriptional modifications driven by STING activation in polarizing TH1 and Th9 cells

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Effect of IL-7 on CD4+ T cell and Th9 cells

Project description:We found that IL-7 pretreatment enhanced Th9 differentiation. To clarify the underlying mechanisms, we examine the gene expression profiles of CD4+ T cell and Th9 cells with or without IL-7 pretreatment. In Th9 cells, we found that Th9 related genes were greatly increased in IL-7 Th9 group, which demonstrated an enhanced Th9 differentiation. In CD4+ T cells, we found that IL-7 treatment resulted in a global gene expression change especially on chromatin remodeling related genes, which facilitated the entry of transcriptional factor to the Il9 promoter region and promoted Il9 transcription.

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Batf3 programs CD8 T cell memory

Project description:Anti-viral CD8 T cell responses are characterized by an initial activation/priming of T lymphocytes followed by a massive proliferation, subset differentiation, population contraction and the development of a stable memory pool. The transcription factor BATF3 has been shown to play a central role in the development of conventional dendritic cells (cDC1), which in turn are critical for the optimal priming of CD8 T cells. Here we show that BATF3 is expressed within the first days after priming but has long-lasting T cell intrinsic effects. We found that T cells that lack Batf3 show a normal expansion and differentiation, yet succumbed to an aggravated contraction and had a diminished memory response. Vice versa BATF3-overexpression in CD8 T cells promoted their survival and transition to memory. Mechanistically, BATF3 regulates T cell apoptosis and longevity via the proapoptotic factor BIM. By programing CD8 T cell survival and memory, BATF3 is a promising molecule to optimize adoptive T cell therapy in patients.

2020-08-31 | GSE143504 | GEO

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