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The transcription factor IRF4 regulates the differentiation and function of intestinal ILC3s.

ABSTRACT: To investigate the role of IRF4 in the regulation of ILC3 development and function, we used the IRF4flox/floxRorccre mice and C57BL/6 mice(6-8 weeks-old ) to carry out single-cell RNA sequencing (BD Rhapsody) on gut ILC3s.

ORGANISM(S): Mus musculus

PROVIDER: GSE271288 | GEO | 2025/06/09

REPOSITORIES: GEO

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The transcription factor IRF4 regulates the differentiation and function of intestinal ILC3s

Project description:To investigate the role of IRF4 in the regulation of ILC3 development and function, we used the wildtype mice as control and carried out single-cell RNA sequencing (BD Rhapsody) on gut ILC3s.

2025-06-09 | GSE281331 | GEO

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

Project description: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.

2023-06-07 | GSE208733 | GEO

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 (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

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.

2022-06-28 | GSE204698 | GEO

NKp46+ ILC3s promote early neutrophil defense against C. difficile infection through GM-CSF secretion

Project description:Clostridioides difficile infection (CDI) is a common cause of antibiotic-associated colitis. C. difficile proliferates and produces toxins that damage the colonic epithelium, leading to symptoms ranging from mild diarrhea to severe pseudomembranous colitis. The host's innate response to CDI occurs in two phases: an early phase in which neutrophils reduce the bacterial load, and a late phase involving repair mechanisms to restore epithelial integrity. Group 3 innate lymphoid cells (ILC3s) are crucial in protecting the gut from CDI. Previous studies have shown that ILC3 production of IL-22 is essential in the late phase of CDI for epithelial repair and maintaining an intestinal microbiota that competes with C. difficile, preventing its expansion. Our study finds that ILC3s also protect during the early stages of CDI by sustaining neutrophils through GM-CSF. Less neutrophil production, accumulation and activation was evident in ILC3-deficient mice than in wild-type (WT) mice, which led to exacerbated symptoms, impaired pathogen clearance, a compromised epithelial barrier, and increased mortality. The adoptive transfer of ILC3s into ILC3-deficient mice restored neutrophil responses and improved disease outcomes. Both in vitro and in vivo experiments revealed that GM-CSF production by ILC3s is crucial for neutrophil production and effective resistance during CDI. Using mice lacking NKp46+ ILC3s, we found that this subset significantly contributes to GM-CSF production in CDI. These findings highlight the critical role of the ILC3-neutrophil connection in early innate responses to CDI. Enhancing ILC3 production of GM-CSF could be a promising strategy for improving host defense against CDI and other enteric infections.

2024-10-17 | GSE277716 | GEO

Microarray data from human cultured ILC3s

Project description:Innate lymphoid cells (ILCs) are tissue-resident lymphocytes subdivided into ILC1s, ILC2s and ILC3s based on core regulatory programs and signature cytokines secreted. ILCs exhibit functional plasticity: for instance, human IL-22-producing ILC3s convert into IFN-γ-producing ILC1-like in vitro. Whether this conversion occurs in vivo is unclear. Using flow cytometry, mass cytometry and scRNAseq, here we found that ILC3s and ILC1s occupy opposite ends of a spectrum including discrete subsets in human tonsils. RNA velocity suggested strong directionality toward ILC1s for one ILC3-ILC1 intermediate cluster. Clonal analysis revealed graded ability of ILC3-ILC1 subsets to convert into ILC1-like cells. When examined in humanized mice, ILC3 acquisition of ILC1 features showed tissue-dependency. In chromatin studies, Aiolos emerged as a nuclear factor that cooperates with Tbet to repress evolutionarily conserved regulatory elements active in ILC3s. The human intestine also exhibited an ILC3–ILC1 transitional population. We conclude that conversion of ILC3s to ILC1-like occurs in vivo in human tissues, and that tissue factors and Aiolos are crucial for this process.

2019-06-18 | GSE132843 | GEO

Functional Targeting of ILC2s and ILC3s reveals selective roles in intestinal fibrosis and homeostasis.

Project description:Innate lymphoid cells (ILCs) are long-lived tissue-resident analogues to T helper cell subsets that lack antigen-specific receptors. Understanding the roles of specific ILC subsets in chronic inflammation and fibrosis has been hampered by a lack of adequate tools for their selective targeting. Here, we used two Cre-deleter strains, Il17rb-CreERT2-eGFP and Rorc-Cre, to selectively delete RORa, a master transcriptional regulator, in ILC2s and ILC3/Th17 cells, respectively. Deletion of RORa in ILC2s led to a significant loss of gastrointestinal ILC2s, a concomitant increase in ILC3s, elevated Th17-type responses, and heightened susceptibility to Crohn’s-like fibrosis in a Salmonella infection model. In contrast, RORa deletion in ILC3/Th17 cells reduced IL-17 production, protecting against fibrosis. We further confirmed the role of IL-17 and ILC3 in fibrotic responses using isolithocholic acid (isoLCA), a microbially-derived secondary bile acid and RORγt inverse agonist. In RORγt reporter and Th17-deficient Rag1−/− mice, isoLCA reduced IL-17 production by ILC3s. In the context of intestinal fibrosis, we show that isoLCA attenuates collagen deposition and fibrotic pathology by dampening RORγt-dependent IL-17 production by ILC3s. These findings reveal a novel interplay between ILC2s and ILC3s in gut homeostasis and demonstrate the therapeutic potential of targeting RORγt in ILC3s as a strategy for preventing fibrosis.

2025-05-15 | GSE290467 | 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

circRNA expression files in ILC3s after DSS treatment

Project description:To explore the role of circRNAs during ILC3-driven colitis, we isolated ILC3s from DSS treated or control Rag1-/- mice. Then circRNA microArray analysis were performed and differentially expressed circRNAs were identified.

2019-12-17 | GSE142106 | GEO

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