Ontology highlight
ABSTRACT:
PROVIDER: PRJNA433909 | ENA |
REPOSITORIES: ENA
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Project description:Runx/Cbfβ complexes protect ILC2s from exhaustion during allergic airway inflammation
| PRJNA438449 | ENA
Project description:Group 2 innate lymphoid cells (ILC2s) have tissue-resident competence and contribute to the pathogenesis of allergic diseases. Therefore, there should be mechanisms to maintain the capacity of ILC2s to produce TH2 cytokines under chronic inflammatory conditions. Here, we report that Runx proteins are essential to prevent exaggerated activation of ILC2, in part by antagonizing GATA-3 function at steady state. However, during allergic inflammation, the absence of Runx in ILC2s impaired their ability to proliferate and produce effector TH2 cytokines and chemokines, but instead induced expression of T cell exhaustion markers including IL-10 and TIGIT. These exhausted ILC2s were unabale to induce type 2 immune responses against repeated allergen inhalation. Thus, Runx proteins protect ILC2s from exhaustion during continuous allergic inflammation.
2019-01-07 | GSE111871 | GEO
Project description:Group-2 innate lymphoid cells (ILC2) are tissue-resident, long-lived innate effector cells implicated in allergy and asthma. Upon activation, mature ILC2 rapidly secret large amounts of type-2 cytokines and other effector molecules. The molecular pathways that drive ILC2 activation are not well understood. Here we report that the transcriptional controller Core-binding factor β (CBFβ) is required for ILC2 activation. Deletion or inhibition of CBFβ did not impair the maintenance of ILC2 at homeostasis, but abolished ILC2 activation during allergic airway inflammation. Treatment with CBFβ inhibitors prevented ILC2-mediated airway hyperresponsiveness in a mouse model of acute Alternaria allergen inhalation. CBFβ promoted expression of key ILC2 genes at both transcriptional and translational levels. CBF transcriptional complex directly bound to Il13 and Vegfa promoters and enhancers, and controlled gene transcription. CBFβ further promoted ribosome biogenesis and enhanced gene translation in activated ILC2. Together, these data establish an essential role for CBFβ in ILC2 activation.
2019-01-23 | GSE116062 | GEO
Project description:<p>Group 2 innate lymphoid cells (ILC2s) play key roles in allergic asthma development. We have previously revealed the inhibitory effect of CD5 antigen-like protein (CD5L) on allergic airway inflammation. Here, we analyzed the effect of CD5L on ILC2s.</p>
2025-09-04 | MTBLS12937 | MetaboLights
Project description:Dietary immunization is vital in regulating allergic airway inflammation mediated by group 2 innate lymphoid cells (ilc2s).
2025-12-30 | GSE294318 | GEO
Project description:Dietary immunization is vital in regulating allergic airway inflammation mediated by group 2 innate lymphoid cells (ilc2s).
2025-12-30 | GSE294316 | GEO
Project description:Type 2 Innate Lymphoid cells (ILC2) play a crucial role in allergic airway inflammation. To identify transcriptional differences between naive ILC2 and allergen induced ILC2, mice were challenged with PBS control or papain on days 0, 3, 6 and 13. On day 14 ILC2 were isolated, sort-purified and sequenced.
2025-12-10 | E-MTAB-15989 | biostudies-arrayexpress
Project description:Type 2 Innate Lymphoid cells (ILC2) play a crucial role in allergic airway inflammation. To identify transcriptional differences between naive ILC2 and allergen induced ILC2, mice were challenged with PBS control or Alternaria alternate on days 0, 3, 6 and 13. On day 14 ILC2 were isolated, sort-purified and sequenced.
2025-12-10 | E-MTAB-15967 | biostudies-arrayexpress
Project description:Stem cell factor (SCF), also known as Kit ligand, is a pleiotropic cytokine that Q5 signals through the c-Kit receptor to regulate cellular development, survival, and proliferation. Although SCF is classically recognized for its essential role in hematopoiesis and mast cell biology, c-Kit is also expressed by innate lymphoid cell progenitors (ILCp) and subsets of mature innate lymphoid cells (ILCs), suggesting broader immunoregulatory functions. Group 2 innate lymphoid cells (ILC2s) are critical mediators of type 2 airway inflammation and serve as an important source of type 2 cytokines during allergic responses. We previously demonstrated increased expression of the pro-inflammatory SCF248 isoform in the lungs of mice with chronic allergic inflammation, while elevated soluble SCF levels have also been reported in patients with asthma. In the present study, we further observed that SCF248 is upregulated in the bone marrow during allergic inflammation, suggesting that SCF248 may contribute to both local and systemic regulation of allergic immune responses. To define the role of SCF/c-Kit signaling in ILC2 biology, we first performed transcriptional profiling of SCF-deficient ILC2s, which revealed reduced expression of genes associated with cytokine signaling, activation, and effector function, including Il4, Stat5b, and PI3K-AKT pathway components, consistent with impaired inflammatory responsiveness. Mechanistically, pro-inflammatory and type 2 cytokines induced SCF248 expression in mesenchymal cells in vitro. To define its functional impact, ILC progenitors were cultured on OP9-DL1 stromal cells with upregulated SCF248 expression, which increased expression of ILC2-associated markers and the maturation program, supporting a role for SCF248 in enhancing ILC2 maturation and activation. In vivo validation using tamoxifen-inducible whole-body SCF-deficient mice (SCFfl/fl; UBC-CreERT2) in an Alternaria alternata model of allergic airway inflammation demonstrated that SCF deficiency reduced SCF248 expression, attenuated type 2 cytokine production, diminished lung inflammation, and decreased circulating and pulmonary ILC2 populations. Similarly, SCF248 blockade reduced allergic inflammation and altered bone marrow ILC compartments. Together, these findings identify SCF248 as a regulator of ILC2 maturation and activation, amplifying mucosal type 2 inflammation during allergic airway disease.
2026-07-01 | GSE336792 | GEO
Project description:Allergic asthma is characterized by type 2 inflammation and overnight worsening of symptoms, yet dynamic fluxes in cellular metabolic profiles driving time-of-day variation remain poorly defined. Group 2 innate lymphoid cells (ILC2s) are central mediators of airway hyperreactivity. We identify melatonin as a previously unrecognized regulator of ILC2 metabolism and function. In murine models of allergic airway inflammation, melatonin reduced eosinophilia, type 2 cytokine production, and airway hyperreactivity without altering ILC2 abundance. Mechanistically, melatonin acted independently of canonical melatonin receptors and instead reprogrammed ILC2 metabolism toward pentose phosphate pathway activity, enhancing NADPH generation and NRF2-dependent glutathione accumulation. Metabolic profiling, loss-of-function approaches, and pharmacologic activation studies demonstrated that NRF2 is both necessary and sufficient to restrain ILC2 effector function. Importantly, primary human ILC2s exhibited conserved NRF2 activation, glutathione accumulation, and reduced type 2 cytokine production in response to melatonin, underscoring clinical relevance. Together, these findings identify the melatonin-NRF2-glutathione axis as a metabolic checkpoint regulating innate type 2 immunity and suggest that therapeutic targeting of redox metabolism may represent a strategy for modulating airway inflammation in allergic asthma.
2026-04-27 | GSE327373 | GEO