Transcriptome analysis of acute IL-33 or chronic HDM activated murine lung ILC2s
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE99780 | GEO | 2020/05/13
REPOSITORIES: GEO
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Project description:The epithelial cell derived cytokines IL-25 and IL-33 can both activate type 2 innate lymphoid cells (ILC2s). It is not known whether the actions of these cytokines on ILC2s are similar or divergent. To investigate this we performed in vitro culture of human ILC2s with a variety of cytokine combinations including IL-2, IL-7, IL-25 and IL-33. Transcriptome profiling of these different condtions allowed us to assess the impact on gene expression of the different treatments. The results show that IL-25 and IL-33 promote divergent gene expression programs indicating that differential expression of these cytokines can cause diverse ILC2 effector function.
2017-08-01 | GSE72433 | 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
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: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
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 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: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.
2013-12-31 | GSE45458 | GEO
Project description:We report the high-throughput profiling of murine intestinal type 2 innate lymphoid cells (ILC2) transcriptome. By obtaining over 8.7 million bases of sequence, we generated genome-wide expression maps of mouse ILC2 without the presense of known activation signals(IL-25, IL-33 receptor) and new non-redundant signal (leukotriene). We find that homeostatic signaling minimally contributes to intestinal ILC2 activation statu. 500 ILC2s were sorted as CD45+Lineage-IL-17RB+
2020-02-16 | GSE144956 | 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 manufacturer’s low sample protocol. A HiSeq 1500 system (Illumina) was used for 50 single-end bases (50SE) sequencing. 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.
2015-10-30 | GSE73272 | GEO
Project description:Group 2 innate lymphoid cells (ILC2s) play critical roles in driving the pathogenesis of allergic airway inflammation. The mechanisms underlying the regulation of ILC2s remain to be fully understood. Here, we identified neuropilin-1 (Nrp1) as a surface marker of ILC2s in response to IL-33 stimulation. Nrp1 was abundantly expressed in ILC2s from lung under steady state, which was significantly reduced upon IL-33 stimulation. ILC2s with high expression of Nrp1 (Nrp1high) displayed lower response to IL-33, as compared with Nrp1low ILC2s. Transcriptional profiling and flow cytometric analysis showed that downregulation of AKT-mTOR signaling participated in the diminished functionality of Nrp1high ILC2s. These observations revealed a potential role of Nrp1 in ILC2s responses under allergic inflammatory condition.
2023-09-30 | GSE243540 | GEO