Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IL-25-induced effector-memory ILC2s mediate small intestinal adaptation [scRNA-Seq 2]

ABSTRACT: This study used single cell RNA sequencing of small intestinal ILC2s +50 days after an IL-25 regimen or PBS regimen in wild type and Il25-/- mice to study memory ILC2 gene signatures.

ORGANISM(S): Mus musculus

PROVIDER: GSE301976 | GEO | 2025/07/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

IL-25-induced effector-memory ILC2s mediate small intestinal adaptation [ATAC-seq]

Project description:This study used bulk ATAC sequencing of either small intestinal ILC2s or Lgr5+ epithelial stem cells +50 days after an IL-25 regimen or PBS regimen in wild type (ILC2s) or Lgr5DTR-EGFP (epithelial stem cells) mice to study chromatin accessibility.

2025-07-28 | GSE301998 | GEO

IL-25-induced effector-memory ILC2s mediate small intestinal adaptation

Project description:This study used bulk ATAC sequencing of epitheilal crypt organoids grown for 6 days, which were isolated from proximal small intestines of wild type mice +50 days after an IL-25 regimen or PBS regimen to study chromatin accessibility.

2025-08-28 | GSE301737 | GEO

IL-25-induced effector-memory ILC2s mediate small intestinal adaptation [scRNA-seq]

Project description:This study used single cell RNA sequencing of small intestinal epitheilal cells +50 days after an IL-25 regimen or PBS regimen in wild type mice to study long-term changes in gene expression by epitheilal cells.

2025-07-28 | GSE301999 | GEO

IL-25-induced effector-memory ILC2s mediate small intestinal adaptation [scRNA-Seq 1]

Project description:This study used single cell RNA sequencing of small intestinal ILC2s +60 days after helminth infection (Nippostrongylus brasiliensis-Nb. or Heligmosomoides polygyrus, Hp.) and in age matched naïve mice (Ctrl) to study memory ILC2 gene signatures after helminth infection.

2025-07-28 | GSE301975 | GEO

Expression data from naive, effector and memory-like ILC2s isolated from mouse lungs and those from effector and memory-like ILC2s isolated from mediastinal lymph node

Project description:Group 2 innate lymphoid cells (ILC2s) in the lung are stimulated by inhaled allergens. ILC2s do not directly recognize allergens but they are stimulated by cytokines including interleukin (IL)-33 released by damaged epithelium.Lung ILC2s, upon stimulation, produce T helper 2 cell-type cytokines inducing T cell independent allergic lung inflammation. We now report that lung ILC2s, upon activation by an allergen or IL-33, acquire the properties of memory cells. The activated ILC2s initially proliferate and secrete cytokines, followed by a contraction phase as they stop producing cytokines. Nevertheless, some persist long after the resolution of the inflammation and acquire intrinsic capacities to react to unrelated allergens more vigorously than naÃ¯ve ILC2s, thus mediating a severe allergic lung inflammation. Gene expression profiles of the previously activated ILC2s show a gene signature of memory T cells. These antigen non-specific memory ILC2s may explain why asthma patients are often sensitized to multiple allergens. ILC2s were isolated from mouse lungs from naive and IL-33 injected mice 4 days, 14 days and 4 months after the initial treatment. RNA was extracted from those ILC2 populations and analyzed for gene expression profiles. RNA was also extracted from ILC2s isolated from lung draining mediastinal lymph node (mLN) 4 days and 14 days after IL-33 treatment.

2016-06-30 | E-GEOD-81700 | biostudies-arrayexpress

Retinoic acid drives intestine-specific adaptation of effector ILC2s originating from distant sites [scRNA-Seq]

Project description:Adaptation of immune cells to tissue-specific microenvironments is a crucial process in homeostasis and inflammation. Here, we show that murine effector type 2 innate lymphoid cells (ILC2s) from various organs are equally effective in repopulating ILC2 niches in other anatomical locations where they adapt tissue-specific phenotypes of target organs. Single-cell transcriptomics of ILC2 populations revealed upregulation of retinoic acid (RA) signaling in ILC2s during adaptation to the small intestinal microenvironment, and RA signaling mediated reprogramming of kidney effector ILC2s towards the small intestinal phenotype in vitro and in vivo. Inhibition of intestinal ILC2 adaptation by blocking RA signaling impaired worm expulsion during Strongyloides ratti infection, indicating functional importance of ILC2 tissue imprinting. In conclusion, this study highlights that effector ILC2s retain the ability to adapt to changing tissue-specific microenvironments, enabling them to exert tissue-specific functions, such as promoting control of intestinal helminth infections.

2023-09-15 | GSE242569 | GEO

Retinoic acid drives intestine-specific adaptation of effector ILC2s originating from distant sites [bulk RNA-Seq]

2023-09-15 | GSE242562 | GEO

IL-25-induced effector-memory ILC2s mediate small intestinal adaptation

Project description:IL-25-induced effector-memory ILC2s mediate small intestinal adaptation

| PRJNA1287499 | ENA

Tuft cell IL-17RB restrains IL-25 bioavailability and reveals context-dependent ILC2 hypoproliferation

Project description:The tuft cell–ILC2 circuit orchestrates rapid type 2 responses upon detecting microbe-derived succinate and luminal helminths. Our findings delineate key mechanistic steps, involving IP3R2 engagement and Ca2+ flux, governing IL-25 production by tuft cells triggered by succinate detection. While IL-17RB plays a pivotal intrinsic role in ILC2 activation, it exerts a regulatory function in tuft cells. Tuft cells exhibit constitutive Il25 expression, placing them in an anticipatory state that facilitates rapid production of IL-25 protein for ILC2 activation. Tuft cell IL-17RB is crucial for restraining IL-25 bioavailability, preventing excessive tonic ILC2 stimulation due to basal Il25 expression. Suboptimal ILC2 stimulation by IL-25 resulting from tuft cell Il17rb-deficiency or prolonged succinate exposure induces a state of hypoproliferation in ILC2s, also observed in chronic helminth infection. Our study offers critical insights into the regulatory dynamics of IL-25 in this circuit, highlighting the delicate tuning required for responses to diverse luminal states.

2025-01-21 | GSE279898 | GEO

IL-25-induced effector-memory ILC2s mediate small intestinal adaptation [ATAC-seq]

Project description:IL-25-induced effector-memory ILC2s mediate small intestinal adaptation [ATAC-seq]

| PRJNA1288253 | ENA