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Pathogen size alters C-type lectin receptor signaling in dendritic cells to influence CD4 Th9 cell differentiation

ABSTRACT: Pathogen size alters C-type lectin receptor signaling in dendritic cells to influence CD4 Th9 cell differentiation

PROVIDER: PRJNA753126 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15382865_1.fastq.gz	Fastqsanger.gz
	SRR15382865_2.fastq.gz	Fastqsanger.gz
	SRR15382866_1.fastq.gz	Fastqsanger.gz
	SRR15382866_2.fastq.gz	Fastqsanger.gz
	SRR15382867_1.fastq.gz	Fastqsanger.gz

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Pathogen size alters C-type lectin receptor signaling in dendritic cells to influence CD4 Th9 cell differentiation

Project description:Dectin-1 recognizes β-glucan in fungal cell walls, and activation of Dectin-1 in dendritic cells (DCs) influences immune responses against fungi. Although many studies have shown that Dectin-1 activated DCs induce different subsets of T helper cells according to different cytokine milieus, the precise mechanisms underlying such differences remain unknown. By harnessing polymorphic Candida albicans and polystyrene beads of different sizes, we found that target size influences production of cytokine that control differentiation of T helper cell subsets. Hyphal C. albicans and large beads activate DCs but cannot be phagocytosed due to their size, which prolongs the duration of Dectin-1 signaling. Transcriptomic analysis revealed that the expression of Il33 was significantly increased by larger targets, and increased IL-33 expression promoted TH9 responses. Expression of IL-33 was regulated by Dectin-1-SYK-PLCγ-CARD9-ERK pathway. Altogether, our study demonstrates that size of fungi can be a determining factor in which DCs induce context-appropriate adaptive immune responses.

2022-04-01 | GSE181734 | GEO

Pathogen size alters C-type lectin receptor signaling in dendritic cells to influence CD4 Th9 cell differentiation.

Project description:Dectin-1 recognizes β-glucan in fungal cell walls, and activation of Dectin-1 in dendritic cells (DCs) influences immune responses against fungi. Although many studies have shown that DCs activated via Dectin-1 induce different subsets of T helper cells according to different cytokine milieus, the mechanisms underlying such differences remain unknown. By harnessing polymorphic Candida albicans and polystyrene beads of different sizes, we find that target size influences production of cytokines that control differentiation of T helper cell subsets. Hyphal C. albicans and large beads activate DCs but cannot be phagocytosed due to their sizes, which prolongs the duration of Dectin-1 signaling. Transcriptomic analysis reveals that expression of Il33 is significantly increased by larger targets, and increased IL-33 expression promotes TH9 responses. Expression of IL-33 is regulated by the Dectin-1-SYK-PLCγ-CARD9-ERK pathway. Altogether, our study demonstrates that size of fungi can be a determining factor in how DCs induce context-appropriate adaptive immune responses.

| S-EPMC9052946 | biostudies-literature

Pathogen size alters C-type lectin receptor signaling in dendritic cells to influence CD4 T cell differentiation

Project description:A key mechanism to eliminate pathogens from the body is the physical internalization (phagocytosis) and degradation of microbes by specialized cells of the immune system including neutrophils, macrophages, and dendritic cells. Phagocytosis not only eliminates potentially harmful pathogens, but also provides information about the “type” of microbe encountered, and helps to orchestrate an appropriate adaptive immune response. Certain pathogens, including filamentous fungi and parasite worms (helminths), exceed the size limit for phagocytosis. In this study we show that when dendritic cells encounter pathogens that are too large to internalize, or when phagocytosis of small microbes is blocked, dendritic cells adopt an activation profile that allows them to orchestrate an adaptive immune response commonly associated with tissue repair and anti-helminth immunity.

2018-10-06 | GSE87670 | GEO

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

Loss of YTHDF2 enhances Th9 programming and CAR-Th9 cell antitumor efficacy

Project description:CD4+ T cells differentiate into various subsets, including T helper 1 (Th1), Th2, Th9, Th17, and regulatory T cells, which are essential in immune responses and cancer immunotherapy. However, the role of RNA N6-methyladenosine (m6A) modification in this differentiation remains unclear. Here, we demonstrate that YTHDF2, a key m6A reader protein known to destabilize m6A-modified mRNA, negatively regulates Th9 cell differentiation. Ablation of Ythdf2 in both mouse and human naïve CD4+ T cells significantly promotes Th9 differentiation by stabilizing Gata3 and Smad3 mRNA under IL-4 and TGF-β signaling. Ythdf2-deficient Th9 cells produce higher levels of IL-9 and IL-21, leading to increased tumor infiltration and cytotoxicity by CD8+ T and NK cells, thereby improving antitumor activity versus wild-type Th9 cells. Moreover, YTHDF2 depletion in CAR-Th9 cells enhances immune activation, reduces terminal differentiation, and augments antitumor efficacy. Targeting YTHDF2 thus represents a promising strategy for enhancing Th9 and CAR-Th9 cell-based cancer immunotherapies.

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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

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.

2014-03-26 | GSE44937 | GEO

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.

2017-02-06 | GSE86542 | GEO

Proteome analysis revealed the essential functions of protein phosphatase PP2A in the induction of Th9 cells

Project description:we performed proteome analysis of Th9 cells to understand the involvement of proteins that might be crucial for the anti-tumor functions of Th9 cells. Here we show for the first time a comprehensive proteomic analysis of murine Th0 and Th9 cells, which identified 1451 total proteins among which 1367 proteins were common. Further analysis revealed that 118 proteins were upregulated while 81 proteins were downregulated in Th9 cells. Pathway analysis suggested an abundance of phosphoproteins in the proteome of Th9 cells. Among upregulated phosphoproteins which showed to be involved in immune 34 system, Ppp2ca (catalytic subunit of protein phosphatase, PP2A) was found to be highly expressed in Th9 cells. Although the role of PP2A has been shown to regulate the differentiation and functions of Th1,Th2, Th17 and Tregs, its role in differentiation and functions of Th9 cells is not identified yet. Our results show for the first time that PP2A is required for the differentiation and anti-tumor functions of Th9 cells. PP2A inhibition leads to the suppression of IL-9 induction and the expression of key transcription factors of Th9 cells.

2021-09-09 | PXD019506 | Pride

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

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