Gene expression data of naïve postnatal day 10 neonatal, naïve adult, and IL-33-activated adult ILC2s isolated from mouse lungs
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PROVIDER: PRJNA625004 | ENA |
REPOSITORIES: ENA
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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 | GSE148539 | GEO
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
Project description:Gene expression data of naïve wildtype and IL-33 knockout ILC2s isolated from adult male mouse lungs
| PRJNA624998 | ENA
Project description:Epidemiological studies have shown sex differences in prevalence of non-allergic asthma. Recent reports demonstrated negative effects of androgen signaling on group 2 innate lymphoid cells (ILC2s), explaining a potential mechanism behind sex bias in asthma prevalence. To further understand the difference in ILC2s based on sex, we have investigated the effects of sex and age on the number and function of lung ILC2s, and epithelium derived cytokines. Naive male and female mice of any ages tested did not differ in the number of ILC2s in the lung. Upon IL-33 injection, lung ILC2s in post puberty female mice responded more vigorously than male counterpart. Purified female lung ILC2s more rapidly produced cytokines than male mouse ILC2s. Gene expression profiles of naïve male and female ILC2s differed in 4% of the genes, and gene set enrichment analysis showed that female ILC2s are enriched for gene signatures of memory T cells. Epithelium-derived cytokines including IL-33 were more highly expressed in post puberty naïve female mouse lungs than male mouse lungs. However, the differences in responsiveness of male and female ILC2s were not affected in IL-33-deficient mice. Therefore, female ILC2s are more readily activated than male ILC2s, likely due to their similarity to memory T cells as suggested by the gene expression profiles.
2019-03-13 | GSE119350 | GEO
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 naïve 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
Project description:To fully characterize the heterogeneity and gene expression profile of mouse lung ILC2s, we generated RORα lineage tracer mice by crossing RoraIRES-Cre (Chou et al., 2013) and R26R-EYFP mice, which have a loxP-flanked stop sequence followed by the gene encoding yellow fluorescent protein (YFP) in the ROSA26 locus. In these RORα-YFP mice, cells expressing Rorα during their development should be irreversibly labeled by YFP. Flow cytometric analyses of lymphocytes in RORα-YFP mice showed that innate lymphoid cells type 2 (ILC2s) were marked by YFP expression. However, both adult and neonatal lung Lin−YFP+ cells were heterogeneous and included not only ILC2s (GATA-3+Thy1+) but also GATA-3−Thy1− and GATA-3lowThy1+ cells. In order to fully assess the lung ILC2 heterogeneity, we analyzed all CD45low/+Linlow cells from adult (6-week-old) and neonatal (12-day-old) RORα-YFP mouse lungs by droplet-based scRNA-seq. Unsupervised clustering of the cells revealed distinct clusters of stromal, B, T, NK cell, DC and ILC2 based on their expression of well-characterized marker genes. We then isolated the ILC2 cluster and performed a second round of unsupervised clustering to examine the existence of possible ILC2 subsets. In both adult and neonatal datasets, ILC2s were divided into subsets with each subset expressing a distinct set of ILC2-associated genes. We validated the existence of distinct ILC2 subsets in adult and neonatal lungs using flow cytometry. We also comprehensively assessed the genes that were specifically and/or differentially expressed by ILC2s compared to other immune and non-immune cell populations in our datasets. This analysis revealed the expression of well-characterized ILC2 genes such as Gata3, Rora, Areg and Il7r as well as other genes with potential immune regulatory functions.
2020-10-27 | GSE123994 | GEO
Project description:Gene expression data of naïve and activated ILC2s isolated from female and male mouse lungs
| PRJNA488822 | ENA
Project description:Gene expression analysis of adult lung ILC2s
| PRJNA510439 | ENA
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 naïve 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.
2016-06-30 | GSE81700 | GEO
Project description:Purpose: We found that IFN-g and IL-27 had suppressive effects on ILC2s cultured with IL-33. The goal of this study is to clarify the expressions of RNA induced by IFN-g and IL-27 in ILC2s. Methods: ILC2s were isolated from fat-asociated lymphid clusters (FALC) of wild-type mice. They were cultured with IL-33 (10ng/ml), IL-33 + IFN-g (10ng/ml), or IL-33 + IL-27 (10ng/ml) for 48hrs. RNA was isolated by Allprep DNA/RNA Micro Kit (QIAGEN), and cDNA libraries were prepared by TruSeq RNA Sample Preparation kits v2 (Illumina) according to the manufacturerâs low sample protocol. A HiSeq 1500 system (Illumina) was used for 50 single-end bases (50SE)ãsequencing. Results: Sequenced reads were trimmed for adaptor sequence, and masked for low-complexity or low-quality sequence, then mapped to the reference genome (mm9) using Bowtie2 v2.1.0 and TopHat2 v2.0.8. The transcript abundances were estimated as FPKM (fragments per kilobase of exon million fragments mapped) value using Cufflinks v2.1.1. We found that both IL-27 and IFN-g upregulated the expression of STAT1 and IRF1 which are regulated downstream of IFN-g receptor signaling, but there was no difference in the expression of GATA3, a critical transcription factor for ILC2 functions. Conclusions: Our study represents the detailed differences of RNA expressions by RNA-seq technology. RNA-Seq analysis of ILC2s cultured with IL-33 (10ng/ml), IL-33 + IFN-g (10ng/ml), or IL-33 + IL-27 (10ng/ml) for 48hrs.
2015-10-30 | E-GEOD-73272 | biostudies-arrayexpress