Transcriptomic changes induced by IL33 transduction, ST2 gene knockout, and their combination in primary mouse lung fibroblasts and unseparated mouse lung cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE197398 | GEO | 2023/01/04
REPOSITORIES: GEO
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Project description:Transcriptomic changes induced by IL33 transduction, ST2 gene knockout, and their combination in primary mouse lung fibroblasts and unseparated mouse lung cells
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Project description:Comparison between WT and ST2 knock-out T-cells upon allogenic stimulation in vitro for 48h
2015-10-14 | E-MEXP-3954 | biostudies-arrayexpress
Project description:Foxp3+ regulatory T cells (Tregs) are critical mediators of peripheral tolerance and immune homeostasis. Tregs that express the IL-33 receptor ST2 are enriched in peripheral nonlymphoid tissues and can exert a variety of tissue-specific functions from metabolic regulation within adipose tissue to skeletal muscle repair. However, the relationship between ST2+ and ST2- Tregs within and across different tissues remains unclear. To compare murine ST2- and ST2+ Tregs within and across tissues, we performed RNA sequencing (RNAseq) of ST2-CD44hi and ST2+CD44hi Tregs from blood, spleen, lungs, visceral adipose tissue (VAT), colon, and skin. RNAseq was also performed on ST2- CD44lo CD62L+ Tregs from the spleen and lungs. We found that the tissue microenvironment was the major factor shaping the transcriptome of Tregs across tissues. Across the tissues studied, Treg transcriptomes displayed an ordered hierarchy that may represent graded levels of activation or differentiation across tissues. We also identified a core signature that distinguished ST2+ Tregs from ST2- Tregs across tissues and a large number of differentially expressed genes between ST2- and ST2+ Tregs within individual tissues that could support the tissue-specific adaptation and function of ST2+ Tregs. In summary, our work highlights the unique, tissue-specific phenotype of ST2+ Tregs and reveals a core ST2+ Treg transcriptional signature shared across tissues.
2022-07-24 | GSE182322 | GEO
Project description:Colorectal cancer (CRC) was induced in Foxp3/eGFP reporter mice by the azoxymethane/dextran sulphate sodium salt (AOM/DSS) protocol. Mice were injected i.p. with the procarcinogen AOM (12.5 mg/kg of body weight). After 1 week, mice received drinking water supplemented with 2.5% DSS for 5 to 7 days, followed by 2 weeks of regular water. The DSS administration was repeated twice with 2% DSS. Mice were sacrificed at week 11 and lamina propia lymphocytes (LPLs) from the colon were isolated. CD4+FOXP3+ (eGFP+) ST2+ or ST2- Tregs were separated from colonic LPLs of CRC induced mice using a FACSAria II cell sorter. Microarray analysis was performed to analyze if ST2+ FOXP3+ Tregs from the colon of CRC mice present a distinct transcription pattern compared to ST2- FOXP3+ Tregs. By this, the role of ST2 for Treg function during intestinal tumorigenesis should be characterized.
2019-05-31 | E-MTAB-6842 | biostudies-arrayexpress
Project description:Severe asthma and sinus disease is a consequence of Type 2 inflammation (T2I), mediated by IL-33 signaling through its membrane-bound receptor, ST2. Soluble (s)ST2 reduces available IL-33 and limits T2I, but little is known about its regulation. We demonstrate that prostaglandin E2 (PGE2) drives production of sST2 to limit features of lung T2I. PGE2 deficient mice display diminished sST2. In humans with severe respiratory T2I, urinary PGE2 metabolites correlate with serum sST2. In mice, PGE2 enhanced sST2 secretion by mast cells (MCs). Mice lacking MCs, ST2 expression by MCs or EP2 receptors by MCs showed reduced sST2 lung concentrations and strong T2I. Recombinant sST2 reduced T2I in mice lacking PGE2 or ST2 expression by MCs back to control levels. PGE2 deficiency also reversed the hyperinflammatory phenotype in mice lacking ST2 expression by MCs. PGE2 thus suppresses T2I through MC-derived sST2, explaining the severe T2I observed in low PGE2 states.
2024-05-20 | GSE266501 | GEO
Project description:Background: Alternaria exposure is associated with severe asthma in humans. Alternaria exposure in mice potently activates group 2 innate lymphoid cells (ILC2s) via the IL-33/ST2 axis and causes ILC2s to robustly secrete type 2 cytokines. Objective: Our aim was to determine whether conventionally used ILC2 markers, ST2 (IL-33R) and CD127 (IL-7Ra), were sufficient to identify all Th2-cytokine producing ILCs after Alternaria exposure. Methods: Mice received intranasal Alternaria for three days prior to analysis. Lung ILCs were identified by flow cytometry as CD45+Lineage−Thy1.2+ lymphocyte-sized cells, divided into four subsets based on ST2 and CD127 expression, and stained for intracellular cytokines and transcription factors. Sort-purified ILC subpopulations were also analyzed by RNA sequencing and qPCR. Results: Alternaria exposure led to accumulation of all ILC populations regardless of ST2 or CD127 expression. Nearly half of the GATA-3+, IL-5+, and IL-13+ ILCs were “unconventional” as they were either single or double negative for ST2/CD127. Further, these populations upregulated CD25, KLRG1, and ICOS after Alternaria challenge. Some activated unconventional IL-5+ ILC2s also produced IFNγ and IL-17A. In addition to shared ILC2 transcripts (Gata3, Il5, Il13) in all populations, RNA-seq further identified novel transcripts enriched in each subset. Finally, transcripts from all populations that correlated best with IL-5 and IL-13 production included Tnfrsf18, Ffar2, and Pde4b. Conclusions: Unconventional ST2- and CD127-negative mouse lung ILC2 populations are induced by Alternaria. Thus, commonly used lung ILC2 identification methods based on ST2 and CD127 do not accurately account for the total ILC2 burden and may exclude nearly half of these cells.
2019-08-22 | GSE136156 | GEO
Project description:Regulatory T cells (Tregs) are enriched in the tumor microenvironment (TME) and suppress anti-tumor immunity. However, the origin of tumor-infiltrating (TI) Tregs and the molecular mechanism underlying their TME accumulation are poorly understood. Although IL-33 was reported to regulate the expansion and function of Tregs, its direct role on TI Tregs and its contribution to tumor progression remain uncertain. Firstly, we demonstrated TI Tregs were primarily thymus-derived. More importantly, we found using comparative transcriptome analysis that proliferation-related genes were prominently upregulated in TI Tregs compared with TI CD4+Foxp3− conventional T cells or splenic Tregs of same tumor-bearing mice. One of these genes, ST2, an interleukin-33 (IL-33) receptor, was identified as a potential factor driving Treg accumulation in the TME. Indeed, IL-33-directed ST2 signaling induced the preferential proliferation of TI Tregs and enhanced tumor progression, while genetic deletion of ST2 in Tregs limited their TME accumulation and delayed tumor growth. These data demonstrate the IL-33/ST2 axis in Tregs as one of the critical pathways for the preferential accumulation of thymus-derived Tregs in the TME and suggest the axis as a potential therapeutic target for cancer immunotherapy.
2020-08-12 | GSE152022 | GEO
Project description:Transcriptional profiling of mouse ST2+ and ST2- Tregs across tissues
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Project description:In diabetics, methylglyoxal (MG), a glucose-derived metabolite, plays a noxious role by inducing oxidative stress, which causes and exacerbates a series of complications. With the use of microarray analysis, we comprehensively screened the gene expression profiles of ST2 cells, derived from a multipotent bone marrow stromal cell line, in the presence or absence of oxidative stress induced by100 M-NM-<M methylglyoxal (MG) treatment to charactrize genes related to diabetic complications. Mouse bone marrow stromal cell-line ST2 (RIKEN, Tsukuba, Japan) was cultured in M-NM-1-MEM (Sigma, St. Louis, MO) supplemented with 10% FBS (Sigma), 100 M-NM-<g/ ml penicillin/ streptomycin (ICN Biomedicals, Inc., Aurora, OH) and 100 M-NM-<M methylglyoxal (MG), and maintained at 37M-BM-0C in a humidified atmosphere with 5% CO2. Total RNA was isolated from ST2 cells treated with or without 100 M-NM-<M methylglyoxal (MG) or 1 M-NM-<M of 5-aza-2M-bM-^@M-^Y-deoxycytidine (5-aza-dC) by standard methods with the use of an RNeasy Protect Mini kit (Qiagen KK, Tokyo, Japan) according to the manufacturerM-bM-^@M-^Ys instructions. Cy3, Cy5 differential expression asasy by Mouse 32K Filgen array
2013-11-19 | E-GEOD-52475 | biostudies-arrayexpress
Project description:We describe the effects of Treg ST2 expression on muscle regeneration. We compare regneration from cryo-injured tibialis anterior muscle from Foxp3-Cre/ST2-flox vs Foxp3-Cre mice 8 days post-injury. These analyses from whole muscle provide insight into the role of muscle Tregs in the context of regeneration. The tibialis anterior muscle from male Foxp3-Cre/ST2 flox or Foxp3-Cre/ST2 WT C57BL/6 mice (2 months old) were cryo-injured using a liquid nitrogen chilled metal probe for 8 seconds. 8 days post-injury whole muscle was harvested and snap frozen in liquid nitrogen. Whole muscle was then homogenized directly in TriZol and gene expression profiling was performed on Affymetrix Mouse Gene 1.0 ST Arrays.
2016-01-10 | E-GEOD-76697 | biostudies-arrayexpress