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ILC2 regulate a Pi16+ fibroblast progenitor niche in the pancreas (naïve ILC2 scRNA-seq)

ABSTRACT: Local fibroblast development and densities underpin their role in regulating organ function and inflammation, although it remains unclear how tissue fibroblast topography is controlled in situ. Here we define group 2 innate lymphoid cells (ILC2) as key regulators of fibroblast homeostasis in the pancreas. We show that ILC2 co-localise with Pi16+Dpp4+Ly6c+Il33+ fibroblast progenitors in an interstitial niche of the exocrine pancreas, which demarcates and encapsulates the organ parenchyma. ILC2 specifically regulate the expansion of this progenitor population, while paradoxically also restraining differentiated intra-parenchymal Col15a1+ fibroblasts under inflammatory conditions. These homeostatic circuits reinforce fibroblast numbers after injury and set an inflammatory threshold at steady-state. Hence, ILC2-fibroblast dialogue represents a regulatory node that locally orchestrates tissue homeostasis and pathology.

ORGANISM(S): Mus musculus

PROVIDER: GSE248385 | GEO | 2026/07/03

REPOSITORIES: GEO

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ILC2 regulate a Pi16+ fibroblast progenitor niche in the pancreas (ILC2 bulk RNAseq)

Project description:Local fibroblast development and densities underpin their role in regulating organ function and inflammation, although it remains unclear how tissue fibroblast topography is controlled in situ. Here we define group 2 innate lymphoid cells (ILC2) as key regulators of fibroblast homeostasis in the pancreas. We show that ILC2 co-localise with Pi16+Dpp4+Ly6c+Il33+ fibroblast progenitors in an interstitial niche of the exocrine pancreas, which demarcates and encapsulates the organ parenchyma. ILC2 specifically regulate the expansion of this progenitor population, while paradoxically also restraining differentiated intra-parenchymal Col15a1+ fibroblasts under inflammatory conditions. These homeostatic circuits reinforce fibroblast numbers after injury and set an inflammatory threshold at steady-state. Hence, ILC2-fibroblast dialogue represents a regulatory node that locally orchestrates tissue homeostasis and pathology.

2026-07-03 | GSE248384 | GEO

ILC2 regulate a Pi16+ fibroblast progenitor niche in the pancreas (acute pancreatitis scRNA-seq)

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ILC2 regulate a Pi16+ fibroblast progenitor niche in the pancreas (coculture bulk RNA-seq)

2026-07-03 | GSE248383 | GEO

ILC2 regulate a fibroblast progenitor niche in the pancreas (Dpp4CreERT2 lineage trace scRNA-seq)

Project description:Local fibroblast development and densities greatly influence organ health and disease, although it remains unclear how tissue fibroblast topography is controlled in situ. Here we define group 2 innate lymphoid cells (ILC2) as key regulators of fibroblast homeostasis in the pancreas. ILC2 co-localise with Pi16+Dpp4+Ly6c+ fibroblasts in an interstitial niche of the exocrine pancreas, which encapsulates the organ parenchyma. ILC2 specifically regulate the expansion of Pi16+Dpp4+Ly6c+ fibroblasts, which have progenitor capacity, while paradoxically also restraining differentiated intra-parenchymal Col15a1+ fibroblasts during inflammation. These homeostatic circuits reinforce fibroblast numbers after injury and set an inflammatory threshold. The ILC2-Pi16+Dpp4+Ly6c+ fibroblast progenitor niche expands locally in cancer, and controls cancer associated fibroblast ontogeny and density. Hence, ILC2-fibroblast dialogue represents a regulatory node that locally orchestrates tissue homeostasis and pathology.

2026-07-03 | GSE308872 | 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.

2022-12-22 | PXD038792 | Pride

Amino acid availability acts as a metabolic rheostat to determine the magnitude of ILC2 responses - SLC7A5 and SLC7A8 KO

2022-12-22 | PXD038786 | Pride

Bulk RNA-Seq of lung Type 2 Innate Lymphoid cells (ILC2) in response to papain

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2025-12-10 | E-MTAB-15989 | biostudies-arrayexpress

Human ILC2 cells stimulated with IL-25, IL-33, or TSLP

Project description:ILC2 cells are a newly described cell type whose biology and contribution to disease are poorly understood. ILC2 cells are activated by allergens, viral infection, and/or epithelial damage via IL-33 and IL-25. ILC2 cells require IL-2, IL-7, IL-25 and IL-33 for their survival and expansion. In mice, ILC2s produce multiple mediators primarily associated with type 2 inflammation (IL-13, IL-5, IL-4, IL-6, IL-9, IL-10, GM-CSF, amphiregulin). ILC2 cells may contribute to the pathology of asthma through multiple mediators that include IL-13-independent pathways. Our goal is to compare transcriptional profiles of IL-33- or IL-25-activated ILC2 cells from blood to characterize these cells and to identify marker(s) that can be utilized to detect them in human tissue. ILC2 cells (Lineage negative, CRTH2+, CD161+, CD127+) were purified from human blood of 5 different donors by flow cytometry. The ILC2 yield ranged from 20,000 to 165,000 cells per donor (0.001-0.008% WBC). Purified ILC2s were expanded in vitro in the presence of IL-2, IL-7, IL-33 and IL-25 (each at 50 ng/ml) for 7-10 days. Expanded cells maintained the ILC2 phenotype (Lineage negative, CRTH2+, CD161+, CD127+). The cells were rested for 2 days in the presence of 1 ng/ml IL-2 and IL-7 and then treated in the presence of 1 ng/ml IL-2 and IL-7 with either media control, IL-25 (50 ng/ml), IL-33 (50 ng/ml), and/or TSLP (50 ng/ml) in combination, for 6 or 24 hours. Whole RNA was isolated via the RNeasy kit (Qiagen). Stratagene Universal Human Reference RNA was used as the reference.

2013-12-31 | E-GEOD-45458 | biostudies-arrayexpress

Expression data of ILC2 cells from Ets1-deleted and littermate control mice

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2016-04-01 | E-GEOD-79742 | biostudies-arrayexpress

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