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Effect of IL-17R in Paneth cells after DSS challenge

ABSTRACT: Effect of IL-17R in Paneth cells after DSS challenge

PROVIDER: PRJEB50556 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR8274490.fastq.gz	Fastqsanger.gz
	ERR8274491.fastq.gz	Fastqsanger.gz
	ERR8274486.fastq.gz	Fastqsanger.gz
	ERR8274487.fastq.gz	Fastqsanger.gz
	ERR8274488.fastq.gz	Fastqsanger.gz

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Effect of IL-17R in Paneth cells after DSS challenge

Project description:Mice with Paneth cell specific genetic ablation of IL-17 receptor and their WT littermates were treated with DSS (dextran sulfate sodium). Ileum tissue was used for RNA Sequencing.

2022-02-02 | E-MTAB-11380 | biostudies-arrayexpress

Intestinal IL-17R signaling controls liver inflammation by constraining microbiome-induced TLR9 signaling and IL-18 production

Project description:IL-17 and IL-17R signaling in the intestinal epithelium regulate the intestinal microbiome. Given the reported links between intestinal dysbiosis, bacterial translocation, and liver disease, we hypothesized that intestinal IL-17R signaling plays a critical role in mitigating hepatic inflammation. To test this, we studied intestinal epithelial-specific IL-17RA deficient mice in a model of concanavalin A hepatitis. Absence of enteric IL-17RA signaling exacerbated hepatitis and hepatocyte cell death. These mice exhibited commensal dysbiosis, increased intestinal and liver Il18, and increased liver translocation of bacterial products, specifically CpG DNA. Mechanistically, CpG DNA induced hepatic IL-18, increasing IFNγ and FasL in hepatic T-cells to drive inflammation. Thus, intestinal IL-17R regulates translocation of TLR9 ligands and constrains susceptibility to hepatitis. These data connect enteric Th17 signaling and the microbiome in hepatitis, with broader implications on the effects of impaired intestinal immunity and subsequent release of microbial products seen in other extra-intestinal pathologies.

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Systematic analysis of IL-17 receptor signalosome reveals a robust regulatory feedback loop

Project description:IL-17 mediates immune protection from fungi and bacteria as well as it promotes autoimmune pathologies. However, the regulation of the signal transduction from the IL-17 receptor (IL-17R) remained elusive. We developed a novel mass spectrometry-based approach to identify components of the IL-17R complex followed by analysis of their roles using reverse genetics. Besides the identification of LUBAC as an important signal transducing component of IL-17R, we established that IL-17 signaling is regulated by a robust negative feedback loop mediated by TBK1 and IKKε. These kinases terminate IL-17 signaling by phosphorylating the adaptor ACT1 leading to the release of the essential ubiquitin ligase TRAF6 from the complex. NEMO recruits both kinases to the IL-17R complex, documenting that NEMO has an unprecedented negative function in IL-17 signaling, distinct from its role in NF-κB activation. Our study provides a comprehensive view of the molecular events of the IL-17 signal transduction and its regulation.

2020-07-15 | PXD019020 | Pride

RNA-seq of mouse ileum to investigate the role of IL-17 receptor signaling in Paneth cells in their biology and intestinal physiology

Project description:IL-17 receptor plays a major role in the antibacterial defense and regulation of host-microbiota interaction. However its impact on Paneth cells, cell-type specific for production of antibacterial peptides, is still not clear. Here, we used genetic depletion of IL-17 receptor specific for Paneth cell population (Defa6-iCre x Il17ra-flox) and performed the RNA sequencing on FACS-sorted Paneth cells and also complete ileum tissue, comparing Cre+ and Cre- littermates.

2022-01-01 | E-MTAB-10038 | biostudies-arrayexpress

CMTM4 is a subunit of the IL-17 receptor and mediates autoimmune pathology

Project description:Interleukin-17A (IL-17A) is a key mediator of protective immunity to yeast and bacterial infections but also drives the pathogenesis of several autoimmune diseases, such as psoriasis or psoriatic arthritis. Here, we show that the tetra-transmembrane protein CMTM4 is a subunit of the IL-17 receptor (IL-17R). CMTM4 constitutively associated with IL-17R subunit C (IL-17RC) to mediate its stability, posttranslational modification, and plasma membrane localization. Both mouse and human cell lines deficient in CMTM4 were largely unresponsive to IL-17A, due to their inability to assemble the IL-17 receptor signaling complex. Accordingly, CMTM4-deficient mice were largely resistant to experimental psoriasis. Collectively, our data identified CMTM4 as an essential component of the IL-17 receptor and a potential therapeutic target for treating IL-17-mediated autoimmune diseases.

2022-12-02 | PXD036366 | Pride

Intestinal IL-17R signaling controls liver inflammation by constraining microbiome-induced TLR9 signaling and IL-18 production

Project description:Intestinal IL-17R signaling controls liver inflammation by constraining microbiome-induced TLR9 signaling and IL-18 production

| PRJNA527218 | ENA

IkappaBzeta Controls IL-17-triggered Gene Expression Program in Intestinal Epithelial Cells that Prevents Expansion of SFB and Attenuates Autoimmune Disorders [jejunum]

Project description:Control of gut microbes is crucial for not only local defense in the intestine but also proper systemic immune responses. Although intestinal epithelial cells (IECs) play important roles in cytokine-mediated control of enterobacteria, the underlying mechanisms are not fully understood. Here we show that deletion of IkappaBzeta in IECs in mice leads to dysbiosis with marked expansion of segmented filamentous bacteria (SFB), thereby enhancing Th17 cell development and exacerbating autoimmune inflammatory diseases. Mechanistically, the IkappaBzeta deficiency results in Paneth cell loss and impaired expression of IL-17-inducible genes involved in IgA production. The Paneth cell loss is caused by aberrant activation of IFN-gamma signaling and a failure of IL-17-mediated recovery from IFN-gamma-induced damage. Thus, the IL-17R–IkappaBzeta axis in IECs contributes to the maintenance of intestinal homeostasis by serving as a key component in a regulatory loop consisting of the gut microbiota and immune cells

2022-12-07 | GSE188252 | GEO

IkappaBzeta Controls IL-17-triggered Gene Expression Program in Intestinal Epithelial Cells that Prevents Expansion of SFB and Attenuates Autoimmune Disorders [ilea]

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IkappaBzeta Controls IL-17-triggered Gene Expression Program in Intestinal Epithelial Cells that Prevents Expansion of SFB and Attenuates Autoimmune Disorders [ATAC-Seq]

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Optimal human intestinal organoid model reveals interleukin-22-induced Paneth cell differentiation

Project description:Here, we developed an optimal system for culturing human small intestinal organoids (hSIOs) that recapitulate the structural and functional complexity of the intestinal crypt in vitro, including mature Paneth cells. With this model, we found that IL-22 is required for the differentiation of human Paneth cells. Rather than STAT3, the PI3K-mTORC1 axis, downstream of IL-22, mediates Paneth cell differentiation programs. CD-associated variants of the IL-22 receptor (IL10RB) were introduced in our system, resulting in the abolishment of Paneth cells in hSIOs. Moreover, our data demonstrated that long-term IL-22 exposure inhibited the growth of hSIOs, challenging the current perception of IL-22 in promoting intestinal regeneration, but rather in reducing cell viability. As a proof-of-principle, our study demonstrates that this optimal culture system for hSIOs has great potential for modelling human intestinal physiology and pathophysiology.

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