ST2 signaling orchestrates mast cell transcriptional activation during viral infection
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE298700 | GEO | 2026/03/13
REPOSITORIES: GEO
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Project description:The role of meningeal mast cells in meningeal antiviral immunity has been poorly studied. Here we investigated the important role of meningeal mast cells in combating LCMV viral infection.
2026-03-13 | GSE263668 | GEO
Project description:ST2 signaling orchestrates mast cell transcriptional activation during viral infection
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Project description:The IL-33/ST2 pathway is important as part of the type 2 immune response against helminth infections. Mast cells express the highest levels of the IL-33 receptor subunit ST2 of any immune cell, and mast cells can mediate type 2 immune inflammation, however the role of IL-33-driven mast cell responses in helminth infection is poorly understood. We sought to determine the role of mast cell ST2 expression during Heligmosomoides polygyrus bakeri (Hpb) infection by generating mast cell conditional ST2 knockout (MCPT5Cre x ST2f/f ,cKO) mice. These mice have normal frequencies of mast cells at steady state, but show specific and strong (albeit incomplete) knockdown of ST2 expression on mast cells. On Hpb infection, faecal egg and adult worm burden were similar between cKO and littermate controls, as were mast cell degranulation markers, serum IgE and goblet cell hyperplasia. Therefore, we conclude that mast cell ST2 does not play a dominant role in Hpb infection. To further investigate the immune response to infection in cKO and littermate controls, transcriptomic and proteomic changes were assessed in duodenal tissues in infected versus naïve mice in cKO and control mice. Minimal transcriptomic and proteomic changes were seen between genotypes, whereas substantial changes were seen between naïve and infected mice, regardless of genotype. Hpb infection induced local increases at the transcript and protein level for mast cell proteases (MCPT1 and MCPT2), resistin-like molecules (RELMα and RELMβ), and markers such as the phospholipase PLA2G4C and the pore-forming protein gasdermin C. Bulk proteomic analysis was also searched against the Hpb genome to identify Hpb proteins present in the duodenal tissues. A list of 60 Hpb proteins of interest were identified in infected duodenal samples, of which 18 contain a signal peptide and are present in the excretory/secretory products of Hpb (HES) (likely secretory products including immunomodulatory proteins); 28 proteins are present in HES but do not contain a signal peptide (likely excretory products); and 14 proteins are not present in HES (likely proteins present in the remnants of Hpb within the duodenum). This work thus provides datasets for changes in the mouse intestine due to Hpb infection, at both the transcript and protein level, as well as a dataset of Hpb proteins detectable in the mouse duodenum at day 14 of infection.
2026-04-06 | PXD074451 | Pride
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:The IL-33/ST2 pathway is important as part of the type 2 immune response against helminth infections. Mast cells express the highest levels of the IL-33 receptor subunit ST2 of any immune cell, and mast cells can mediate type 2 immune inflammation, however the role of IL-33-driven mast cell responses in helminth infection is poorly understood. We sought to determine the role of mast cell ST2 expression during Heligmosomoides polygyrus bakeri (Hpb) infection by generating mast cell conditional ST2 knockout (MCPT5Cre x ST2f/f, cKO) mice. These mice have normal frequencies of mast cells at steady state, but show specific and strong (albeit incomplete) knockdown of ST2 expression on mast cells. On Hpb infection, faecal egg and adult worm burden were similar between cKO and littermate controls, as were mast cell degranulation markers, serum IgE and goblet cell hyperplasia. Therefore, we conclude that mast cell ST2 does not play a dominant role in Hpb infection. To further investigate the immune response to infection in cKO and littermate controls, transcriptomic and proteomic changes were assessed in duodenal tissues in infected versus naïve mice in cKO and control mice. Minimal transcriptomic and proteomic changes were seen between genotypes, whereas substantial changes were seen between naïve and infected mice, regardless of genotype. Hpb infection induced local increases at the transcript and protein level for mast cell proteases (MCPT1 and MCPT2), resistin-like molecules (RELMα and RELMβ), and markers such as the phospholipase PLA2G4C and the pore-forming protein gasdermin C. Bulk proteomic analysis was also searched against the Hpb genome to identify Hpb proteins present in the duodenal tissues. A list of 60 Hpb proteins of interest were identified in infected duodenal samples, of which 18 contain a signal peptide and are present in the excretory/secretory products of Hpb (HES) (likely secretory products including immunomodulatory proteins); 28 proteins are present in HES but do not contain a signal peptide (likely excretory products); and 14 proteins are not present in HES (likely proteins present in the remnants of Hpb within the duodenum). This work thus provides datasets for changes in the mouse intestine due to Hpb infection, at both the transcript and protein level, as well as a dataset of Hpb proteins detectable in the mouse duodenum at day 14 of infection.
2026-03-09 | GSE315703 | GEO
Project description:The role of meningeal stromal cells in meningeal antiviral immunity has been poorly studied. Here we investigated the response of meningeal stromal cells in combating LCMV viral infection.
2026-03-13 | GSE263665 | 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:Mast Cells Control Lung Type 2 Inflammation via Prostaglandin E2-Driven Soluble ST2.
| PRJNA1107468 | ENA
Project description:IL-33/ST2 signaling plays a crucial role in macrophage function during kidney injury. Using myeloid cell-specific ST2 knockout mice, the study revealed that ST2 deficiency attenuates renal damage in acute IRI but exacerbates it in chronic IRI. RNAseq and functional assays showed that ST2 is critical for macrophage-mediated efferocytosis and mitochondrial metabolism. The findings highlight the importance of IL-33/ST2 signaling in regulating macrophage activity and maintaining tissue homeostasis during renal injury.
2026-03-04 | GSE288154 | GEO
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