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ILC2 regulate a Pi16+ fibroblast progenitor niche in the pancreas (coculture bulk RNA-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: GSE248383 | 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 (naïve ILC2 scRNA-seq)

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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.

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The embryonic origins of site-specific arthritis; Bulk RNA sequencing of CD34+(Pi16+) fibroblasts stimulated with TNF and IL1b.

Project description:The cellular basis for site-specific inflammation remains unclear. In human fingers, proximal interphalangeal (PIP) joints are preferentially affected by inflammatory arthritis, whereas distal interphalangeal (DIP) joints are spared, providing a model to investigate the predilection of inflammation to distinct sites. We combine single-cell RNA sequencing, imaging and X-ray tomography to examine cellular composition, spatial organization and structure of finger joints during foetal development. PIP joints were enriched for Pi16+ fibroblasts, which are located in perivascular regions and at tendon–ligament interfaces. To investigate whether Pi16+ fibroblasts have a specific response to inflammatory cytokines Pi16+ and Pi16- cells were sorted from foetal fingers using the co-expressed marker CD34. Thes cells were cultured in vitro with and without TNF and IL1b and analyzed using bulk RNA sequencing.

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Histological Signatures Reveal Anti-Fibrotic Factors in Mouse and Human Lungs [scRNA-seq]

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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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