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Cxxc finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging [Cxxc1 KO CUT&TAG]

ABSTRACT: To investigate the role of Cxxc1 in the regulation of ILC3 development and function, we carry out cleavage under targets and tagmentation (CUT&Tag) to characterize the genome-wide profiles of the H3K4me3 modification on Cxxc1flox/floxRorccre and Cxxc1flox/flox ILC3s.

ORGANISM(S): Mus musculus

PROVIDER: GSE211017 | GEO | 2023/06/07

REPOSITORIES: GEO

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Cxxc finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging (Cxxc1-deficient mice)

Project description:To investigate the role of Cxxc1 in the regulation of ILC3 development and function, we used Cxxc1flox/floxRorccre mice and carried out single-cell RNA sequencing (BD Rhapsody) on small intestinal ILC3s.

2023-06-07 | GSE209592 | GEO

Cxxc finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging [H3K4me3]

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Cxxc finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging

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Group 3 innate lymphoid cells continuously require the transcription factor GATA3 after commitment

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2015-11-23 | E-GEOD-71198 | biostudies-arrayexpress

Cxxc finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging [control scRNA-seq]

Project description:To investigate the role of aging in the regulation of ILC3 development and function, we used the young mice as control and carried out single-cell RNA sequencing (BD Rhapsody) on young gut ILC3s.

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Metabolite - sensing receptor Ffar2 regulates colonic group 3 innate lymphoid cells and gut immunity

Project description:Group 3 innate lymphoid cells (ILC3s) sense environmental signals that are critical for gut homeostasis and host defense. However, the metabolite-sensing G-protein-coupled receptors that regulate colonic ILC3s remain poorly understood. We found that colonic ILC3s expressed Ffar2, a microbial metabolite-sensing receptor, and that Ffar2 agonism promoted ILC3 expansion and function. Deletion of Ffar2 in ILC3s decreased their in situ proliferation and ILC3-derived IL-22 production. This led to impaired gut epithelial function characterized by altered mucus-associated proteins and antimicrobial peptides and increased susceptibility to colonic injury and bacterial infection. Ffar2 increased IL-22+ CCR6+ ILC3s and influenced ILC3 abundance in colonic lymphoid tissues. Ffar2 agonism differentially activated AKT or ERK signaling and increased ILC3-derived IL-22 via an AKT and STAT3 axis. Our findings demonstrate that Ffar2 regulates colonic ILC3 proliferation and function in a cell-intrinsic manner and identifies an ILC3-receptor signaling pathway regulating gut inflammatory tone and pathogen defense.

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Group 3 innate lymphoid cells amplify YAP1-driven small intestinal repair

Project description:Ror gamma t-deficient mice lack group 3 Innate Lymphoid Cells (ILC3s) and as a result have increased tissue damage and diminished tissue repair in response to insult. To identify repair programs associated with ILC3 presence the transcriptomes of small intestinal stem cells exposed to damage in the presence or absence of ILC3 were compared. Small intestinal damage was induced in Ror gamma t-deficient Lgr5 reporter mice and littermate controls. Small intestinal epithelial stem cells were purified at days 1 and 4 after damage and subjected to RNA sequencing.

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Group 3 innate lymphoid cells continuously require the transcription factor GATA3 after commitment

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Group 3 innate lymphoid cell pyroptosis represents a host defense mechanism against Salmonella infection

Project description:Group 3 innate lymphoid cells (ILC3s) produce interleukin (IL)-22 and, together with other cells in the gut, orchestrate to mount productive host immunity against bacterial infection. However, the role of ILC3s in Salmonella enterica serovar Typhimurium (S. Typhimurium) infection, which causes foodborne enteritis in humans, remains elusive. Here, we show that S. Typhimurium exploit ILC3-produced IL-22 to promote its infection. Specifically, S. Typhimurium secrete flagellin through activation of the TLR5-Myd88-IL-23 signaling pathway in antigen presenting cells (APCs) to selectively enhance IL-22 production by ILC3s, but not T cells. Deletion of ILC3s but not T cells in mice led to better control of S. Typhimurium infection. We also show that S. Typhimurium can invade ILC3s directly and cause caspase-1-mediated ILC3 pyroptosis independently of flagellin. Genetic ablation of Casp1 in mice leads to increased ILC3 survival and IL-22 production, and enhanced S. Typhimurium infection. Collectively, our data suggest a key host defense mechanism against S. Typhimurium infection via induction of ILC3 death to limit intracellular bacteria and reduce IL-22 production.

2022-05-23 | GSE201292 | GEO

Group 3 innate lymphoid cells mediate early protective immunity against Mycobacterium tuberculosis

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2019-05-11 | GSE131031 | GEO

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