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Fate mapping reveals a prenatal-to-neonatal wave of ILC2s with a history of Cd3g expression

ABSTRACT: Group 2 innate lymphoid cells (ILC2s) are thought to develop in the bone marrow and fetal liver. However, increasing evidence supports the presence of thymic ILC2s in mice and humans. In this study, we introduce a novel fate-mapping mouse model designed to track thymic ILC2s in peripheral tissues. Thymic ILC2s are labeled by ZsGreen whose expression is induced by Cd3giCre. While they are present in the thymus and peripheral tissues, they are not found in the bone marrow. These cells are predominantly abundant during the neonatal stage, when the intense alveolarization and tissue remodeling occur. RNA sequencing revealed elevated expression of cytokine genes, Il13 and Il4, as well as Klrg1 in these cells. They also harbor TCR gene rearrangements suggesting common developmental pathways with T cells. Furthermore, we demonstrate that neonatal ILC2s play a critical role in macrophage polarization in a naphthalene-induced injury lung model. These findings help explore the differences between pediatric and adult immunity and future therapeutic strategies.

ORGANISM(S): Mus musculus

PROVIDER: GSE326669 | GEO | 2026/04/07

REPOSITORIES: GEO

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Fate mapping reveals a prenatal-to-neonatal wave of ILC2s with a history of Cd3g expression - RNA-Seq

Project description:Group 2 innate lymphoid cells (ILC2s) are thought to develop in the bone marrow and fetal liver. However, increasing evidence supports the presence of thymic ILC2s in mice and humans. In this study, we introduce a novel fate-mapping mouse model designed to track thymic ILC2s in peripheral tissues. Thymic ILC2s are labeled by ZsGreen whose expression is induced by Cd3giCre. While they are present in the thymus and peripheral tissues, they are not found in the bone marrow. These cells are predominantly abundant during the neonatal stage, when the intense alveolarization and tissue remodeling occur. RNA sequencing revealed elevated expression of cytokine genes, Il13 and Il4, as well as Klrg1 in these cells. They also harbor TCR gene rearrangements suggesting common developmental pathways with T cells. Furthermore, we demonstrate that neonatal ILC2s play a critical role in macrophage polarization in a naphthalene-induced injury lung model. These findings help explore the differences between pediatric and adult immunity and future therapeutic strategies.

2026-04-06 | GSE326762 | GEO

Mus musculus

Project description:Neonatal bone marrow stroma

| PRJNA309405 | ENA

Down-regulation of E protein activity augments an ILC2 differentiation program in the thymus

Project description:Innate lymphoid cells (ILCs) are important regulators in various immune responses. Current paradigm states that all newly-made ILCs originate from common lymphoid progenitors (CLP) in the bone marrow. Id2, an inhibitor of E protein transcription factors, is indispensable for ILC differentiation. Unexpectedly, we found that ectopically expressing Id1 or deleting two E protein genes in the thymus drastically increased ILC2 counts in the thymus and other organs where ILC2 normally reside. Further evidence suggests a thymic origin of these mutant ILC2s. The mutant mice exhibit augmented spontaneous infiltration of eosinophils and heightened responses to papain in the lung and increased ability to expulse the helminth parasite, Nippostrongylus brasiliensis. These results prompt the question whether the thymus naturally has the capacity to produce ILC2s and E proteins restrain such a potential. The abundance of ILC2s in Id1 transgenic mice also offers a unique opportunity for testing the biological functions of ILC2s.

2017-02-08 | GSE94597 | GEO

Suppression of ILC2 differentiation from committed T cell precursors by E protein transcription factors

Project description:Current models propose that group 2 innate lymphoid cells are generated in the bone marrow. Here we demonstrate that subsets of these cells can differentiate from multipotent progenitors and committed T cell precursors in the thymus, both in vivo and in vitro. These thymic ILC2s can exit the thymus, circulate in the blood and home to peripheral tissues. Ablation of E protein transcription factors greatly promotes the innate lymphoid cell fate at the expense of B and T cell development. Consistently, a transcriptional network centered on the ZBTB16 transcription factor and IL-4 signaling pathway is highly up-regulated due to E protein deficiency. Our results show that ILC2 can still be generated from what are normally considered to be committed T cell precursors, and that this alternative cell fate is restrained by high levels of E protein activity in these cells.

2019-01-20 | GSE111518 | GEO

Altered Metabolomics and Inflammatory Transcriptomics in Human Bone Marrow Adipocytes After Acute High Calorie Diet and Acute Fasting

Project description:Investigated bone marrow metabolism in response to acute overnutrition (high calorie diet) and calorie deprivation (fasting). Bone marrow serum and peripheral serum were collected before and after each dietary intervention. Using proteomics analyses of the sera, we characterized nutritional influences on the local and systemic environments. In brief, proteomic analysis of the bone marrow serum after high calorie diet showed an upregulation of proteins related to an inflammatory/complement pathway, while bone marrow serum after fasting showed a significant downregulation of inflammatory/complement pathway proteins. In contrast, the peripheral serum showed signs of an increased inflammatory response that may be due to a rapid increase in body weight and fat mass seen in participants after 10 days of a high calorie diet. After fasting, peripheral serum did show a strong inflammatory response, but there was evidence of increased lipid biosynthesis. Overall, our results demonstrate key differences in inflammatory response and lipid metabolism between high calorie diet and fasting, despite a nearly identical bone marrow adipose phenotype.

2025-07-14 | PXD063552 | Pride

Gene expression data of naïve wildtype and IL-33 knockout ILC2s isolated from adult male mouse lungs

Project description:Group 2 innate lymphoid cells (ILC2s) in mouse lungs are activated by the epithelium-derived alarmin IL-33. Activated ILC2s proliferate and produce IL-5 and IL-13 that drive allergic responses. In neonatal lungs, IL-33 is spontaneously released resulting in activation of lung ILC2s. Here we report that neonatal lung ILC2 activation has significant effects on ILC2 functions in adulthood. Most neonatal lung ILC2s incorporated bromodeoxyuridine (BrdU) and persisted into adulthood. BrdU+ ILC2s in adult lungs responded more intensely to IL-33 treatment than BrdU- ILC2s. In IL-33 deficient (KO) mice, lung ILC2s develop normally but they are not activated in the neonatal period. Lung ILC2s in KO mice responded less intensely to IL-33 in adulthood compared to wild type (WT) ILC2s. While there was no difference in the number of lung ILC2s, there were fewer IL-13+ ILC2s in IL-33KO than IL-33WT mice. The impaired responsiveness of ILC2s in KO mice was reversed by intranasal injections of IL-33 in the neonatal period. These results suggest that activation of lung ILC2s by endogenous IL-33 in the neonatal period may “train” ILC2s seeding the lung after birth to become long-lasting resident cells that respond more efficiently to challenges later in life.

2020-04-14 | GSE148545 | GEO

Gene expression data of naïve postnatal day 10 neonatal, naïve adult, and IL-33-activated adult ILC2s isolated from mouse lungs

2020-04-14 | GSE148539 | GEO

Gene expression profiling of bone marrow and lung ILC2s

Project description:We found that CD45, a membrane bound tyrosine phosphatase important for T cell development, negatively regulated ILC2s in a cell-intrinsic manner. ILC2s in CD45-deficient mice exhibited enhanced proliferation and maturation in bone marrow and hyperactivated phenotypes in lung with alteration of cell metabolism.

2023-07-28 | GSE212115 | GEO

Gene expression profiling of bone marrow and lung ILC2s

Project description:Gene expression profiling of bone marrow and lung ILC2s

| PRJNA874038 | ENA

The neural crest is a source of mesenchymal stem cells with specialized hematopoietic stem-cell-niche function

Project description:Mesenchymal stem cells (MSCs) And osteolineage cells contribute to the hematopoietic stem cell (HSC) Niche in the bone marrow of long bones. However, Their developmental relationships remain unclear. Here we demonstrate that different MSC populations in the developing marrow of long bones have distinct functions. Proliferative mesoderm-derived nestin- MSCs participate in fetal skeletogenesis, And lose MSC activity soon after birth. In contrast, Quiescent neural-crest-derived nestin+ Cells in the same bones preserve MSC activity, But do not generate fetal chondrocytes. Instead, They differentiate into HSC-niche-forming MSCs, Helping to establish the HSC niche by secreting Cxcl12. Perineural migration of these cells to the bone marrow requires the ErbB3 receptor. The neonatal Nestin-GFP+ PDGFR- Cell population also contains Schwann-cell precursors, But does not comprise mature Schwann cells. Thus, In the developing bone marrow HSC-niche-forming MSCs share a common origin with sympathetic peripheral neurons and glial cells, And ontogenically distinct MSCs have non-overlapping functions in endochondrogenesis and HSC niche formation. Total RNA was isolated from small numbers of FACS sorted stromal cells, obtained from neonatal Nes-Gfp bone marrow preparations (2 biological replicates). Each independent set of samples was obtained from pooled skeletal elements (long bones and sterna) form multiple littermates.

2014-10-15 | E-GEOD-61695 | biostudies-arrayexpress

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