Co-culture of murine small intestinal organoids with type-3 innate lymphoid cells (ILC3)
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ABSTRACT:
PROVIDER: PRJNA1019731 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26142445_1.fastq.gz | Fastqsanger.gz | |||
| SRR26142445_2.fastq.gz | Fastqsanger.gz | |||
| SRR26142446_1.fastq.gz | Fastqsanger.gz | |||
| SRR26142446_2.fastq.gz | Fastqsanger.gz | |||
| SRR26142447_1.fastq.gz | Fastqsanger.gz |
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Project description:Type-3 innate lymphoid cells (ILC3) regulate homeostasis and orchestrate immunity in the intestine, mediated in part by their bi-directional communication with the intestinal epithelium. In order to define specific interactions between these two compartments, we used a reductionist co-culture system of murine epithelial small intestinal organoids (SIO) with ILC3. The transcriptomic profile of epithelial cells from these co-cultures was analysed by bulk RNAseq.
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Project description:Innate lymphoid cells (ILC) are tissue-resident effector cells with important roles in tissue homeostasis, protective immunity and inflammatory disease. Current nomenclature divides ILC into subsets based on the expression of master transcription factors and effector cytokine programs. In mucosal barrier tissues, group 3 ILC (ILC3) have been defined by the expression of the master transcription factor RORgt. However, ILC3 can be further subdivided into two major subsets – natural cytotoxicity receptor-expressing (NCR+) ILC3 and lymphoid tissue inducer (LTi)-like ILC3 which share type 3 effector modules but also exhibit significant ontological, transcriptional, phenotypic and functional heterogeneity. In particular, LTi-like ILC3 exhibit effector functions not typically associated with other RORgt-expressing lymphocytes, provoking the hypothesis that other master transcription factors may contribute to LTi-like ILC3 biology. Here we identify Bcl6 as an LTi-like ILC3 associated transcription factor in both mice and humans. Deletion of Bcl6 led to dysregulation of the LTi-like ILC3 transcriptional program and changes to subset-specific phenotypic markers and effector functions. Strikingly, loss of Bcl6 enhanced expression of the type 3 effector cytokines IL-17A and IL-17F in LTi-like ILC3, which was found to be in part dependent upon the commensal microbiota. Together these findings implicate Bcl6 as an ILC3 subset-defining transcription factor and part of a network that confers phenotype and function on LTi-like ILC3. Our study further provides a missing link to redefine analogous immune modules in innate and adaptive lymphocyte responses.
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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.
2018-06-29 | E-MTAB-6639 | biostudies-arrayexpress
Project description:Small intestinal group 3 innate lymphoid cells (ILC3) from ILC3-conditional BMAL1 knock out mice or littermate control mice were sort-purified for transcriptional analysis
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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. 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.
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2019-03-14 | E-MTAB-7088 | biostudies-arrayexpress
Project description:How group 3 innate lymphoid cells (ILC3) regulate mucosal protection in the presence of T cells remains poorly understood. Here, we examined ILC3 function in intestinal immunity using ILC3-deficient mice that maintain endogenous T cells, Th17 cells, and secondary lymphoid organs. ILC3 were dispensable for generation of Th17 and Th22 cell responses to commensal and pathogenic bacteria, and absence of ILC3 did not affect IL-22-production by CD4 T cells before or during infection. However, despite presence of IL-22-producing T cells, ILC3 and ILC3-derived IL-22 were required for maintaining homeostatic functions of the intestinal epithelium. T cell-sufficient, ILC3-deficient mice were capable of pathogen clearance and survived infection with low dose Citrobacter rodentium. However, ILC3 increased pathogen tolerance at early timepoints of infection by activating tissue-protective immune pathways. Consequently, ILC3 were indispensable for survival of high dose infection. Our results demonstrate a crucial context-dependent role for ILC3 in immune-sufficient animals and provide a blueprint for uncoupling of ILC3 and Th17 cell functions.
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Project description:Group 3 innate lymphoid cells (ILC3) are composed of NCR- and NCR+ subsets located at mucosal sites exposed to billions of commensal microbes and potentially harmful pathogens. Together with T cells, the various ILC3 subsets maintain the balance between homeostasis and immune activation. Using genetic mapping, we reveal here the existence of a new subset of NCR- ILC3 transiently expressing Ncr1 but strongly related to unlabeled NCR- ILC3, demonstrating previously unsuspected heterogeneity within the NCR- ILC3 population. Notch signaling is required for the differentiation of NCR- ILC3 into NCR+ ILC3. However, we show here that Notch signaling must be sustained for the maintenance of the NCR+ phenotype and that TGF-β impairs the development of NCR+ ILC3. Thus, ILC3 diversity and the plasticity of the NCR- and NCR+ subsets is regulated by the balance between the opposing effects of Notch and TGF-β signaling, maintaining homeostasis in the face of continual challenges. Transcriptional profiling of three ILC subsets (NCR-FM-, NCR-FM- and NCR+FM+) using RNA sequencing
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