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Gene expression profile at single cell level of Innate Lymphoid Cells (ILCs), Natural Killer (NK) cells , and T cells from human tonsils

ABSTRACT: Gene expression profile at single cell level of Innate Lymphoid Cells (ILCs), Natural Killer (NK) cells , and T cells from human tonsils

PROVIDER: PRJNA952912 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24092228.fastq.gz	Fastqsanger.gz
	SRR24092229.fastq.gz	Fastqsanger.gz

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Gene expression profile after freeze-thawing at single cell level of Innate Lymphoid Cells (ILCs), Natural Killer (NK) cells , and T cells from human tonsils

Project description:Gene expression profile after freeze-thawing at single cell level of Innate Lymphoid Cells (ILCs), Natural Killer (NK) cells , and T cells from human tonsils

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Gene expression profiling of small intestine (SI) NKp46+RORgt+ and NKp46+RORgt- Innate Lymphoid Cells (ILCs)

Project description:The aim of this study was to analyze the global transcriptional profiles of small intestine (SI) Innate Lymphoid Cells (ILCs) expressing the NK cell marker NKp46. Based on differential expression of the RORgt transcription factor SI NKp46+ ILCs can be divided in NKp46+RORgt- and NKp46+RORgt+ cells. While NKp46+RORgt- cells produce IFN-g, like conventional Natural Killer (NK) cells, NKp46+RORgt+ cells secrete IL-22, like Lymphoid Tissue inducer (LTi) cells. We compared the global transcriptional profiles of both NKp46+RORgt- and NKp46+RORgt+ cells to conventional splenic NK cells and to SI NKp46-RORgt+ cells, which contain adult LTi cells. By following this approach, we showed that SI NKp46+RORγt- ILCs correspond to SI NK cells. We also identified a transcriptional program conserved in adult SI NKp46+RORγt+, NKp46-RORγt+ ILCs and fetal LTi. The various ILC cell populations analyzed in this study were isolated from C57BL/6 RORc(gt)+/GFP reporter mice. SI NKp46+RORγt- (NKp46+GFP-) cells, SI NKp46+RORγt+ cells (NKp46+GFPlow and NKp46+GFPhigh cells) and NKp46-RORγt+ ILCs, including adult LTi cells , were sorted by flow cytometry from CD3- lamina propria cells of small intestine (SI) of RORc(γt)+/GFP reporter mice . Splenic NKp46+RORγt- (NKp46+GFP-) cells were also sorted as the reference for conventional NK cells. Two replicates of each populations were produced and analyzed.

2011-06-20 | E-GEOD-29777 | biostudies-arrayexpress

Single cell RNA-sequencing of human tonsil Innate lymphoid cells (ILCs)

Project description:Single cell RNA-sequencing of human tonsil Innate lymphoid cells (ILCs) from three independent tonsil donors. Sequencing libraries were prepared from FACS sorted individual ILCs with the Smart-Seq2 protocol (Picelli et al. Nature Methods 2013)

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Distinct Gene Regulatory Pathways for Human Innate Versus Adaptive Lymphoid Cells [ChIP-seq & ATAC-seq]

Project description:Innate lymphoid cells (ILCs) serve as sentinels in mucosal tissues, sensing release of soluble inflammatory mediators, rapidly communicating danger via cytokine secretion, and functioning as guardians of tissue homeostasis. Although ILCs have been studied extensively in model organisms, little is known about these âfirst respondersâ in humans, especially their lineage and functional kinships to cytokine-secreting T helper cell (Th) counterparts. Here, we report gene regulatory circuitries for four human ILCâTh counterparts derived from mucosal environments, revealing that each ILC subset diverges as a distinct lineage from Th and circulating natural killer cells, but shares circuitry devoted to functional polarization with their Th counterparts. Super-enhancers demarcate cohorts of cell identity genes in each lineage, uncovering new modes of regulation for signature cytokines, novel molecules that likely impart important functions to ILCs, and potential mechanisms for autoimmune disease SNP associations within ILCâTh subsets. Molecular profiling of innate lymphoid and T helper cells subsets purified from tonsils and NK cells purified from peripheral blood using Assay for Transposase-Accessible Chromatin (ATAC) and chromatin immunoprecipitation (H3K4me3 and H3K27ac).

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Gene expression profiling of small intestine (SI) NKp46+RORgt+ and NKp46+RORgt- Innate Lymphoid Cells (ILCs)

2011-06-20 | GSE29777 | GEO

Gene expression profile at single cell level of Innate Lymphoid Cells (ILCs), Natural Killer (NK) cells , and T cells from human tonsils

Project description:We used single cell RNA sequencing to investigate the diversity of ILCs, NKs, and T cells in the human tonsil

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Single cell RNA-sequencing of human tonsil Innate lymphoid cells (ILCs)

Project description:Single cell RNA-sequencing of human tonsil Innate lymphoid cells (ILCs) from three independent tonsil donors.

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Gene expression profile after freeze-thawing at single cell level of Innate Lymphoid Cells (ILCs), Natural Killer (NK) cells , and T cells from human tonsils

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RNA-binding protein RBM3 negatively regulates innate lymphoid cells (ILCs) and lung inflammation

Project description:Innate lymphoid cells (ILCs) promote lung inflammation in diseases such as asthma through cytokine production. RNA-binding proteins (RBPs) are critical post-transcriptional regulators of cellular function though the role of RBPs in innate lymphoid cells is unknown. Here, we demonstrate that RNA-binding motif 3 protein (RBM3) is one of the most highly expressed RBPs in Thy1.2+ lung ILCs after fungal allergen challenge and is further induced by epithelial cytokines TSLP and IL-33 in both human and mouse ILCs. Single (rbm3-/-) and double (rbm3-/-rag2-/-) knockout mice exposed via the airway to the asthma-associated fungal allergen Alternaria alternata displayed increases in eosinophilic lung inflammation and ILC activation compared to control mice. In addition to increased Th2 cytokine production, rbm3-/- ILCs produced elevated IL-17A. The negative regulation by RBM3 in ILC responses was direct as purified rbm3-/- ILCs were hyperinflammatory in vitro and in vivo after stimulation with IL-33. Transcriptomic analysis by RNA-sequencing of rbm3-/- lung ILCs showed increased type 2 and 17 cytokines as well as global expression differences in critical cytokines, receptors, transcription factors, and survival transcripts compared with WT ILCs. Importantly, these transcript changes were independent of the numbers of AU-rich elements (AREs) which RBM3 is known to bind. Thus, regulation of ILC responses by RNA-binding proteins offers novel mechanistic insight into lung ILC biology and ILC-driven inflammatory diseases.

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Project description:We previously found that while CCR10+ ILCs are dominant in the healthy skin, they differentiate into CCR10- ILCs in the skin of mice with various dysregulated or inflammatory conditions, such as T/B cell-deficient Rag1-/- mice. These suggest that CCR10- ILCs are activated effector cells in response to altered skin environments. To gain clues about the functional mechanism and regulation of the ILC activation in the skin, we compared gene expression profiles of CCR10+ skin ILCs of wild-type (WT) mice versus CCR10- or CCR10low skin ILCs of WT and Rag1-/- mice using microarray analyses. Skin innate lymphoid cells were isolated by BD FACSAria sorting system. The microarry was perfomanced by Immunological Genome Project using Affymetrix arrays and used for analysis of gene expresssion of CCR10+ ILCs and CCR10- ILCs in different mice species as indicated.

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