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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE208733 | 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.

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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.

2023-06-07 | GSE210193 | GEO

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

Project description:To investigate the role of aging 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 aged and young gut ILC3s.

2023-06-07 | GSE210194 | GEO

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

Project description: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.

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

Project description:GATA3 is indispensable for the development of all IL-7RÎ±-expressing innate lymphoid cells (ILCs) and maintenance of type 1 ILCs (ILC1s) and type 2 ILCs (ILC2s). However, the importance of low GATA3 expression in type 3 ILCs (ILC3s) is still elusive. Here, we report that GATA3 regulates homeostasis of ILC3s by controlling IL-7RÎ± expression. In addition, GATA3 is critical for the development of NKp46+ ILC3 subset partially through regulating the balance between T-bet and RORÎ³t. Genome-wide analyses indicate that while GATA3 positively regulates CCR6+ and NKp46+ ILC3 subset-specific genes in respective lineages, it negatively regulates CCR6+ ILC3-specific genes in NKp46+ ILC3s. Furthermore, GATA3 regulates IL-22 production in both CCR6+ and NKp46+ ILC3s. Thus, low GATA3 expression is critical for the development and function of ILC3 subsets. To identify GATA3 regulated genes in total ILC3s with RNA-Seq; To identify unique genes expressed by CCR6+ ILC3 or NKp46+ ILC3 and GATA3 regulated genes within these two ILC3 subsets with RNA-Seq; To identify GATA3 direct binding sites in ILC3s, ILC2s and Th2 cells with ChIP-Seq.

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

The Transcription Factor ThPOK Regulates ILC3 Lineage Homeostasis and Function during Intestinal Infection II

Project description:To investigate the role of ThPOK in the regulation of ILC3 development and function, we established conventional ThPOK knockout mice and carried out single-cell RNA sequencing (BD Rhapsody) on intestinal 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.

2019-09-16 | GSE137508 | GEO

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

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2018-06-29 | E-MTAB-6639 | biostudies-arrayexpress

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

Project description:GATA3 is indispensable for the development of all IL-7Rα-expressing innate lymphoid cells (ILCs) and maintenance of type 1 ILCs (ILC1s) and type 2 ILCs (ILC2s). However, the importance of low GATA3 expression in type 3 ILCs (ILC3s) is still elusive. Here, we report that GATA3 regulates homeostasis of ILC3s by controlling IL-7Rα expression. In addition, GATA3 is critical for the development of NKp46+ ILC3 subset partially through regulating the balance between T-bet and RORγt. Genome-wide analyses indicate that while GATA3 positively regulates CCR6+ and NKp46+ ILC3 subset-specific genes in respective lineages, it negatively regulates CCR6+ ILC3-specific genes in NKp46+ ILC3s. Furthermore, GATA3 regulates IL-22 production in both CCR6+ and NKp46+ ILC3s. Thus, low GATA3 expression is critical for the development and function of ILC3 subsets.

2015-11-23 | GSE71198 | GEO

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

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