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Tissue signals imprint ILC2 identity with anticipatory function

ABSTRACT: Tissue signals imprint ILC2 identity with anticipatory function

PROVIDER: PRJNA482471 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR7549270.fastq.gz	Fastqsanger.gz
	SRR7549280.fastq.gz	Fastqsanger.gz
	SRR7549290.fastq.gz	Fastqsanger.gz
	SRR7549300.fastq.gz	Fastqsanger.gz

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Tissue signals imprint ILC2 identity with anticipatory function [RNA-Seq]

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Tissue signals imprint ILC2 identity with anticipatory function [RNA-Seq]

Project description:Group 2 innate lymphoid cells (ILC2s) are distributed systemically and produce type 2 cytokines in response to a variety of stimuli, including the epithelial cytokines interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP). Transcriptional profiling of ILC2s from different tissues, however, grouped ILC2s according to their tissue of origin, even in the setting of combined IL-25, IL-33R and TSLPR-deficiency. Single-cell profiling confirmed a tissue-organizing transcriptome and identified ILC2 subsets expressing distinct activating receptors, including the major subset of skin ILC2s, which were activated preferentially by IL-18. Tissue ILC2 subsets were normal in germ- free mice, suggesting that endogenous, tissue-derived, signals drive the maturation of ILC2 subsets by controlling expression of distinct patterns of activating receptors, thus anticipating tissue-specific patterns to perturbations occurring later in life.

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Tissue signals imprint ILC2 identity with anticipatory function [single cell RNA-Seq]

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Tissue signals imprint ILC2 identity with anticipatory function.

Project description:Group 2 innate lymphoid cells (ILC2s) are distributed systemically and produce type 2 cytokines in response to a variety of stimuli, including the epithelial cytokines interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP). Transcriptional profiling of ILC2s from different tissues, however, grouped ILC2s according to their tissue of origin, even in the setting of combined IL-25-, IL-33-receptor-, and TSLP-receptor-deficiency. Single-cell profiling confirmed a tissue-organizing transcriptome and identified ILC2 subsets expressing distinct activating receptors, including the major subset of skin ILC2s, which were activated preferentially by IL-18. Tissue ILC2 subsets were unaltered in number and expression in germ-free mice, suggesting that endogenous, tissue-derived signals drive the maturation of ILC2 subsets by controlling expression of distinct patterns of activating receptors, thus anticipating tissue-specific perturbations occurring later in life.

| S-EPMC6202223 | biostudies-literature

Tissue signals imprint ILC2 identity with anticipatory function

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-09-10 | GSE117568 | GEO

Amino acid availability acts as a metabolic rheostat to determine the magnitude of ILC2 responses - WT ILC2

Project description:Group 2 innate lymphoid cells (ILC2) are functionally poised, tissue-resident lymphocytes that respond rapidly to damage and infection at mucosal barrier sites. ILC2 reside within complex microenvironments where they are subject to cues from both the diet and invading pathogens – including helminths. Emerging evidence suggests ILC2 are acutely sensitive not only to canonical activating signals, but also perturbations in nutrient availability. In the context of helminth infection, we identify amino acid availability as a nutritional cue in regulating ILC2 responses. ILC2 were found to be uniquely pre-primed to import amino acids via the large neutral amino acid transporters Slc7a5 and Slc7a8. Cell-intrinsic deletion of these transporters individually impaired ILC2 expansion, while concurrent loss of both transporters markedly impaired the proliferative and cytokine producing capacity of ILC2. Moreover, amino acid determined the magnitude of ILC2 responses in part via tuning of mTOR. These findings implicate essential amino acids as a metabolic requisite for optimal ILC2 responses within mucosal barrier tissues.

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Project description:We report the high-throughput profiling of murine intestinal type 2 innate lymphoid cells (ILC2) transcriptome. By obtaining over 8.7 million bases of sequence, we generated genome-wide expression maps of mouse ILC2 without the presense of known activation signals(IL-25, IL-33 receptor) and new non-redundant signal (leukotriene). We find that homeostatic signaling minimally contributes to intestinal ILC2 activation statu. 500 ILC2s were sorted as CD45+Lineage-IL-17RB+

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Transcription factor Bcl11b controls identity and function of mature innate lymphoid cells type II

Project description:Type-2 innate lymphoid cells (ILC2s) promote anti-helminth responses and contribute to allergies. Though Bcl11b has been previously considered a T-lineage identity transcription factor (TF) that restrains the innate-cell genetic programs, we report here that Bcl11b is highly expressed in mature ILC2s and acts upstream of the key ILC2 TFs Gfi1, Gata-3, and of IL-33 receptor IL1rl1 (T1ST2). Additionally, Bcl11b-/- ILC2s de-repressed Rorγt, Ahr and IL-23 receptor, normally expressed in type-3 ILCs (ILC3s). Consequently, Bcl11b-/- ILC2s lost ILC2 functions and gained ILC3 functions, expanding in response to the protease allergen papain, however producing IL-17 and IL-22, and not IL-5 and IL-13, causing lung neutrophilia rather than eosinophilia, and diminished mucus production. Our results broaden Bcl11b's role from a T-cell only TF, and establishes that Bcl11b sustains mature ILC2 genetic and functional programs and lineage fidelity through positive regulation of essential ILC2 TFs and negative regulation of pivotal ILC3 TFs. RNA-seq analysis on sorted ILC2s from the mLNs of Bcl11bF/F Cre-ERT2 and wildtype mice at steady state following tamoxifen mediated deletion of Bcl11b

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