Expression data of RANKL-deficient CCR6+ ILC3
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ABSTRACT:
PROVIDER: PRJNA448769 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Microarrays were used to determine transcriptional differences between CCR6+ ILC3s isolated from RorccreTnfsf11fl/fl and Tnfsf11fl/fl small intestine lamina propria.
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Project description:Microarray data of REV-ERBa-deficient CCR6+ ILC3
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Project description:Microarray was used to determine transcriptional differences between Nr1d1+/+ CCR6+ ILC3s and Nr1d1-/- CCR6+ ILC3s isolated from small intestine lamina propria
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Project description:Group 3 innate lymphoid cells (ILC3s) play a crucial role in intestinal inflammatory disorders such as necrotizing enterocolitis (NEC) in neonates; however, the mechanisms by which ILC3s contribute to NEC remain unclear. In this study, single-cell transcriptomics, in vivo experiments on T cell-deficient mice, and targeted cell interventions demonstrated that NKp46−CCR6− (double-negative, DN) ILC3 autophagy significantly impacts NEC development by regulating intracellular metabolism. Mice lacking ATG5 or treated with autophagy inhibitors exhibited reduced ILC3 abundance and impaired ILC3 function, alleviating NEC. Mechanistically, ATG5 deficiency enhanced fatty acid metabolism while reducing glycolysis. Conversely, inhibiting fatty acid oxidation or supplementing with lactate restored the quantity and functionality of ATG5-deficient DN ILC3s, exacerbating NEC. Lipid metabolism analyses combined with a mouse model of NEC indicated that phosphatidylcholine supplementation alleviated intestinal inflammation by inhibiting DN ILC3 autophagy. Clinically, patients with NEC showed elevated ILC3 levels and significant enrichment of autophagy genes. These findings highlight the importance of DN ILC3 autophagy in metabolic adaptation, suggesting potential strategies for managing NEC.
2026-04-12 | GSE306522 | GEO
Project description:Group 3 innate lymphoid cells (ILC3s) play a crucial role in intestinal inflammatory disorders such as necrotizing enterocolitis (NEC) in neonates; however, the mechanisms by which ILC3s contribute to NEC remain unclear. In this study, single-cell transcriptomics, in vivo experiments on T cell-deficient mice, and targeted cell interventions demonstrated that NKp46−CCR6− (double-negative, DN) ILC3 autophagy significantly impacts NEC development by regulating intracellular metabolism. Mice lacking ATG5 or treated with autophagy inhibitors exhibited reduced ILC3 abundance and impaired ILC3 function, alleviating NEC. Mechanistically, ATG5 deficiency enhanced fatty acid metabolism while reducing glycolysis. Conversely, inhibiting fatty acid oxidation or supplementing with lactate restored the quantity and functionality of ATG5-deficient DN ILC3s, exacerbating NEC. Lipid metabolism analyses combined with a mouse model of NEC indicated that phosphatidylcholine supplementation alleviated intestinal inflammation by inhibiting DN ILC3 autophagy. Clinically, patients with NEC showed elevated ILC3 levels and significant enrichment of autophagy genes. These findings highlight the importance of DN ILC3 autophagy in metabolic adaptation, suggesting potential strategies for managing NEC.
2026-04-12 | GSE319269 | GEO
Project description:Group 3 innate lymphoid cells (ILC3s) play a crucial role in intestinal inflammatory disorders such as necrotizing enterocolitis (NEC) in neonates; however, the mechanisms by which ILC3s contribute to NEC remain unclear. In this study, single-cell transcriptomics, in vivo experiments on T cell-deficient mice, and targeted cell interventions demonstrated that NKp46−CCR6− (double-negative, DN) ILC3 autophagy significantly impacts NEC development by regulating intracellular metabolism. Mice lacking ATG5 or treated with autophagy inhibitors exhibited reduced ILC3 abundance and impaired ILC3 function, alleviating NEC. Mechanistically, ATG5 deficiency enhanced fatty acid metabolism while reducing glycolysis. Conversely, inhibiting fatty acid oxidation or supplementing with lactate restored the quantity and functionality of ATG5-deficient DN ILC3s, exacerbating NEC. Lipid metabolism analyses combined with a mouse model of NEC indicated that phosphatidylcholine supplementation alleviated intestinal inflammation by inhibiting DN ILC3 autophagy. Clinically, patients with NEC showed elevated ILC3 levels and significant enrichment of autophagy genes. These findings highlight the importance of DN ILC3 autophagy in metabolic adaptation, suggesting potential strategies for managing NEC.
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Project description:Innate lymphoid cells (ILC) are similar to T helper (Th) cells in expression of cytokines and transcription factors. For example, RORγt is the lineage-specific transcription factor for both ILC3 and Th17 cells. However, the ILC counterpart for BCL6-expressing T follicular helper (Tfh) cells has not been defined. Here, we report that in the ILC compartment, BCL6 is selectively co-expressed with not only CXCR5, but also RORγt and CCR6 in ILC3 from multiple tissues. BCL6-deficient ILC3 produce enhanced levels of IL-17A and IL-22. More importantly, phenotypic and single-cell ATAC-seq analysis show that absence of BCL6 in mature ILC3 increases the numbers of ILC1 and transitional cells co-expressing ILC3 and ILC1 marker genes. A lineage-tracing experiment further reveals BCL6+ ILC3 to ILC1 trans-differentiation under steady state. Lastly, microbiota promote BCL6 expression in colonic CCR6+ ILC3, and thus reinforce their stability. Collectively, our data have demonstrated that CCR6+ ILC3 have both Th17 and Tfh programs and that BCL6 expression in these cells functions to maintain their lineage identity.
2022-12-27 | GSE221341 | GEO
Project description:ILC3 contain 3 well-defined subsets, CCR6+ ILC3, NKp46+ ILC3, and CCR6–NKp46– DN ILC3. These subsets had not previously been transcriptionally compared and the extent to which they had shared or unique transcriptional profiles remained unclear. We used microarray to determine transcriptional differences between these 3 subsets and to find putative factors that support the survival of CCR6+ ILC3 during cytokine depletion.
2017-02-10 | GSE92693 | GEO
Project description:Innate lymphoid cells (ILC) are similar to T helper (Th) cells in expression of cytokines and transcription factors. For example, RORγt is the lineage-specific transcription factor for both ILC3 and Th17 cells. However, the ILC counterpart for BCL6-expressing T follicular helper (Tfh) cells has not been defined. Here, we report that in the ILC compartment, BCL6 is selectively co-expressed with not only CXCR5, but also RORγt and CCR6 in ILC3 from multiple tissues. BCL6-deficient ILC3 produce enhanced levels of IL-17A and IL-22. More importantly, phenotypic and single-cell ATAC-seq analysis show that absence of BCL6 in mature ILC3 increases the numbers of ILC1 and transitional cells co-expressing ILC3 and ILC1 marker genes. A lineage-tracing experiment further reveals BCL6+ ILC3 to ILC1 trans-differentiation under steady state. Lastly, microbiota promote BCL6 expression in colonic CCR6+ ILC3, and thus reinforce their stability. Collectively, our data have demonstrated that CCR6+ ILC3 have both Th17 and Tfh programs and that BCL6 expression in these cells functions to maintain their lineage identity.
2022-12-29 | GSE220437 | GEO
Project description:Innate lymphoid cells (ILC) are similar to T helper (Th) cells in expression of cytokines and transcription factors. For example, RORγt is the lineage-specific transcription factor for both ILC3 and Th17 cells. However, the ILC counterpart for BCL6-expressing T follicular helper (Tfh) cells has not been defined. Here, we report that in the ILC compartment, BCL6 is selectively co-expressed with not only CXCR5, but also RORγt and CCR6 in ILC3 from multiple tissues. BCL6-deficient ILC3 produce enhanced levels of IL-17A and IL-22. More importantly, phenotypic and single-cell ATAC-seq analysis show that absence of BCL6 in mature ILC3 increases the numbers of ILC1 and transitional cells co-expressing ILC3 and ILC1 marker genes. A lineage-tracing experiment further reveals BCL6+ ILC3 to ILC1 trans-differentiation under steady state. Lastly, microbiota promote BCL6 expression in colonic CCR6+ ILC3, and thus reinforce their stability. Collectively, our data have demonstrated that CCR6+ ILC3 have both Th17 and Tfh programs and that BCL6 expression in these cells functions to maintain their lineage identity.
2022-12-29 | GSE220434 | GEO