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Intestinal helminth skews dendritic cell development to counter the anti-helminth immune response

ABSTRACT: Intestinal helminth skews dendritic cell development to counter the anti-helminth immune response

PROVIDER: PRJNA1231530 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32569520_1.fastq.gz	Fastqsanger.gz
	SRR32569520_2.fastq.gz	Fastqsanger.gz
	SRR32569521_1.fastq.gz	Fastqsanger.gz
	SRR32569521_2.fastq.gz	Fastqsanger.gz
	SRR32569522_1.fastq.gz	Fastqsanger.gz

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Intestinal helminth skews dendritic cell development to counter the anti-helminth immune response

Project description:Intestinal dendritic cells (DC) orchestrate the adaptive immune response that balances protection against pathogens and tolerance towards harmless antigens. Yet, it remains largely unknown what molecular mechanisms underly this functional duality. Heligmosomoides polygyrus bakeri (Hpb) is a naturally occurring parasite in mice characterised by unique immune-evasion strategies that counter host protective immunity. Here, we utilised this unique infection environment to study mechanisms by which DC maintain the immune balance. In-depth characterisation of intestinal DC during Hpb infection revealed the emergence of distinct populations of DC that drive protective Th2 responses, versus others with immunoregulatory properties. We also identified that the skewing of intestinal DC towards immunoregulatory functions was due to TGFb signalling via endogenous sources or by Hpb-produced TGFb-mimic molecules. Thus, our results present a mechanistic explanation for Hpb’s ability to modulate the adaptive immune system. Furthermore, these data offer an example of how heterogeneity within the DC compartment can determine the simultaneous generation of both pro- and anti-inflammatory immune responses.

2025-03-17 | GSE291087 | GEO

Transcriptomic profile of Tfh cells during intestinal helminth infection

Project description:The goal of this study was to define the regulation of Tfh cell response during intestinal helminth infection. Using the helminth Trichuris muris, we performed RNA-seq analysis on Tfh cells that develop during acute vs chronic helminth infection. We found that the transcriptomic profile of acute vs chronic induced Tfh cells are distinct and they express Th2/Th1-associated genes, respectively.

2021-10-20 | GSE185992 | GEO

Chromatin accessibility profile of Tfh cells during intestinal helminth infection

Project description:The goal of this study was to define the regulation of Tfh cell response during intestinal helminth infection. Using the helminth Trichuris muris, we performed ATAC-seq analysis on Tfh cells that develop during acute vs chronic helminth infection. We found that the epigenetic profile of acute vs chronic induced Tfh cells are distinct by adopting Th2 and Th1 cell phenotypes, respectively. For example, Th2-associated genes such as the Il4 locus was more accessible in acute-induced Tfh cells (and vice versa for Th1-associated genes in chronic-induced Tfh cells).

2021-10-20 | GSE186062 | GEO

ILC3s-derived RANKL contributes to tuft cell hyperplasia and anti-helminth immunity

Project description:Intestinal tuft cells are reported to orchestrate parasite type 2 immunity through producing IL-25 and LTC4. Meanwhile, type 2 cytokines IL-13 and IL-4 can induce tuft cell hyperplasia from intestinal stem cells during helminth infection. Here, using intestinal organoids culture, we show that RANKL synergizes with both IL-13 and IL-4 to enhance tuft cell expansion. Genetic mouse models revealed that RANK-RelB axis in intestinal epithelial cells (IECs) is required for optimal tuft cell-ILC2 circuit activation during helminth infection. Mechanistically, RANKL enhances IL-13-activated IL-4RA/STAT6 signaling in IECs, promoting tuft cell differentiation. Using genetic mouse models, we further demonstrated that ILC3s-derived RANKL is indispensable for optimal tuft cell hyperplasia during helminth infection. The scRNA-seq data revealed that N. brasiliensis infection will modulate ILC3 subsets distribution and RANKL expression.

2025-05-19 | GSE247660 | GEO

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Heme-activated Nrf2 signaling skews fate trajectories of bone marrow cells from dendritic cells towards macrophages

Project description:Heme-activated Nrf2 signaling skews fate trajectories of bone marrow cells from dendritic cells towards macrophages

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Human resistin alters lung mRNA expression from helminth-infected lungs.

Project description:Goal: To examine the effects of human resistin during helminth infection. Methodology: To examine the function of human resistin (hResistin), we utilized transgenic mice expressing the human resistin gene along with its entire regulatory region (hRetnTg+). Following infection with the helminth Nippostrongylus brasiliensis, whole lung RNA was sequenced in hRetnTg+ mice, control hRetnTg- and naïve mice. Conclusion: In hRetnTg+ mice, many genes involved in inflammation and the immune system, specifically toll-like receptor signaling and chemokines, are significantly upregulated, suggesting that human resistin promotes TLR signaling and inflammation during helminth infection. Examination of whole lung mRNA from Nippostrongylus brasiliensis-infected lungs at day 7 in mice expressing human resistin

2014-11-14 | E-GEOD-60537 | biostudies-arrayexpress

Characterization of ST2+ and ST2- mTh cells in helminth infection

Project description:CD4+T cells are differentiated into Th1, Th2, Th17 and Treg cells after Antigen presentation by other cell types such as dendritic cells, macrophages and B cells in Lymph nodes. Those differentiated CD4+T cells are subdivided into cell subsets by their producing cytokines and surface markers. We recently identified that ST2 expressing Th2 cells highly produced IL-5 comparing to ST2- Th2 cells in helminth infection. In this study, we investigated the RNAseq analysis to characterize these Th2 cells.

2018-09-20 | GSE120173 | GEO

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Project description:Consumption of ethanol has detrimental effects on gastric organs such as the intestine. To demonstrate the deleterious effect of alcohol, we sacrificed isobaric feeding or ethanol feeding mice and sorted the dendritic cells from their intestine organ. The dendritic cells were analyzed by a small-scale global proteomics approach. We achieved to obtain the biological signatures in the alcohol abuse mice group using bioinformatics analysis.

2024-06-16 | PXD033700 | Pride

Notch-activated basophils support intestinal CD4+ T cell fate and function during helminth infection

Project description:Helminth infections affect billions of people worldwide and cause substantial morbidity. Intestinal helminth infection provokes Type 2 inflammation orchestrated by CD4+ T helper 2 (Th2) cells. Th2s produce interleukin (IL)-4 and IL-13 that prompt an epithelial “weep and sweep” response to drive parasite clearance. Tissue-specific cues optimize CD4+ T cell responses, but the mechanisms regulating intestinal Th2 responses remain unclear. Previously, we identified that the Notch signaling pathway in basophils, rare granulocytes, drove effective parasite clearance and an optimal Th2 response during Trichurismuris infection, a mouse model of human whipworm. Here we report basophil-intrinsic Notch was required for infection-elicited Th2 cytokine responses and a broader IL-4 production program across intestinal CD4+ T cell subsets. In vitro, basophils supported CD4+ T cell cytokine production in a contact-dependent manner, independent of basophil-secreted factors, and was dependent on autocrine IL-4 production from CD4+ T cells. In vivo, basophil-intrinsic Notch mediated basophil-Th2 cell interactions in the cecum during infection. Thus, Notch-programmed basophils act in a contact-dependent manner to optimize intestinal CD4+ T cell function during helminth infection. These findings improve our understanding of the tissue-specific mechanisms regulating intestinal CD4+ T cell responses at inflamed mucosal barriers during Type 2 immunity.

2025-08-27 | GSE297084 | GEO

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