ArticleAllergy2020
A critical role for c-Myc in group 2 innate lymphoid cell activation.
Article in Allergy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- HuR Regulates GATA3-Driven Type 2 Inflammation in CD4bioRxiv : the preprint server for biology · 2026Article
- Analysis and validation of diagnostic biomarkers and immune cell infiltration characteristics in chronic spontaneous urticaria and autophagy based on machine learning.The World Allergy Organization journal · 2026Article
- Epithelial AhR Suppresses Allergen-Induced Oxidative Stress and Senescence via c-Myc Regulation.Antioxidants (Basel, Switzerland) · 2025Article
- Serine/threonine kinase 33 mediates thrombin-induced interleukin-8 release from human lung epithelial cells in severe asthma.Respiratory research · 2025Article
- Generative prediction of causal gene sets responsible for complex traits.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- MAIT cell deficiency exacerbates neuroinflammation in P301S human tau transgenic mice.Journal of neuroinflammation · 2025Article
- E-cigarette vapor extract alters human eosinophil gene expression in an effect mediated by propylene glycol, glycerin, and nicotine.Journal of leukocyte biology · 2024Article
- Can probiotics be used in the prevention and treatment of bronchial asthma?Pharmacological reports : PR · 2024Review
- MYC: there is more to it than cancer.Frontiers in cell and developmental biology · 2024Review
- CD45 alleviates airway inflammation and lung fibrosis by limiting expansion and activation of ILC2s.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Metabolic regulation by prostaglandin EAllergy · 2023Article
- SLC7A8 is a key amino acids supplier for the metabolic programs that sustain homeostasis and activation of type 2 innate lymphoid cells.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A20 Enhances the Expression of the Proto-Oncogene C-Myc by Downregulating TRAF6 Ubiquitination after ALV-A Infection.Viruses · 2022Article
- Review
- Immunomodulation therapy offers new molecular strategies to treat UTI.Nature reviews. Urology · 2022Review
- Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer.EBioMedicine · 2022Article
- Innate immunity in pancreatic cancer: Lineage tracing and function.Frontiers in immunology · 2022Review
- Demethylzeylasteral inhibits proliferation, migration, and invasion through FBXW7/c-Myc axis in gastric cancer.MedComm · 2021Article
- Group 2 innate lymphoid cells are numerically and functionally deficient in the triple transgenic mouse model of Alzheimer's disease.Journal of neuroinflammation · 2021Article
- Taking the Myc out of cancer: toward therapeutic strategies to directly inhibit c-Myc.Molecular cancer · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAsthma is a complicated chronic inflammatory disorder characterized by airway inflammation and bronchial hyperresponsiveness. Group 2 innate lymphoid cells (ILC2) are tissue-resident innate effector cells that can mediate airway inflammation and hyperresponsiveness through production of IL-5, IL-13 and VEGFA. ILC2 in asthma patients exhibit an activated phenotype. However, molecular pathways that control ILC2 activation are not well understood.
methodsMYC expression was examined in ILC2 sorted from peripheral blood of healthy controls and asthma patients or cultured with or without activating cytokines. CRISPR knockout technique was used to delete c-Myc in primary murine lung ILC2 or an ILC2 cell line. Cell proliferation was examined, gene expression pattern was profiled by genome-wide microarray analysis, and direct gene targets were identified by Chromatin immunoprecipitation (ChIP). ILC2 responses, airway inflammation and airway hyperresponsiveness were examined in Balb/c mice challenged with Alternaria extracts, with or without treatment with JQ1.
resultsILC2 from asthma patients expressed increased amounts of MYC. Deletion of c-Myc in ILC2 results in reduced proliferation, decreased cytokine production, and reduced expression of many lymphocyte activation genes. ChIP identified Stat6 as a direct gene target of c-Myc in ILC2. In vivo inhibition of c-Myc by JQ1 treatment repressed ILC2 activity and suppressed Alternaria-induced airway inflammation and AHR.
conclusionc-Myc expression is upregulated during ILC2 activation. c-Myc is essential for ILC2 activation and their in vivo pathogenic effects. These findings suggest that targeting c-Myc may unlock novel strategies to combat asthma or asthma exacerbation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.