ArticleAllergy2015
Notch signaling mediates granulocyte-macrophage colony-stimulating factor priming-induced transendothelial migration of human eosinophils.
Article in Allergy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The trial behind it
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Notch signaling in the tumor immune microenvironment of colorectal cancer: mechanisms and therapeutic opportunities.Journal of translational medicine · 2025Review
- Unexpected Multiple Gastrointestinal Cancers in a Patient with Chronic Eosinophilia: A Case Report.Journal of gastrointestinal cancer · 2024Article
- Notch 2 signaling contributes to intestinal eosinophil adaptations in steady state and tissue burden following oral allergen challenge.Journal of leukocyte biology · 2024Article
- Molecular pathways underlying lung-brain axis signaling in asthma: Relevance for psychopathology and neuroinflammation.The Journal of allergy and clinical immunology · 2024Article
- β2-Integrins - Regulatory and Executive Bridges in the Signaling Network Controlling Leukocyte Trafficking and Migration.Frontiers in immunology · 2022Review
- The GM-CSF-IRF5 signaling axis in eosinophils promotes antitumor immunity through activation of type 1 T cell responses.The Journal of experimental medicine · 2020Article
- Article
- GM-CSF in inflammation.The Journal of experimental medicine · 2020Review
- An Evaluation of theFrontiers in immunology · 2020Review
- Multi-Faceted Notch in Allergic Airway Inflammation.International journal of molecular sciences · 2019Review
- Notch Signaling Orchestrates Helminth-Induced Type 2 Inflammation.Trends in immunology · 2019Review
- Protective Role of Eosinophils and TNFa after Ozone Inhalation.Research report (Health Effects Institute) · 2017Article
- Notch signaling in lung diseases: focus on Notch1 and Notch3.Therapeutic advances in respiratory disease · 2016Review
- Targeting GM-CSF in inflammatory diseases.Nature reviews. Rheumatology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPriming with cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF) enhances eosinophil migration and exacerbates the excessive accumulation of eosinophils within the bronchial mucosa of asthmatics. However, mechanisms that drive GM-CSF priming are incompletely understood. Notch signaling is an evolutionarily conserved pathway that regulates cellular processes, including migration, by integrating exogenous and cell-intrinsic cues. This study investigates the hypothesis that the priming-induced enhanced migration of human eosinophils requires the Notch signaling pathway.
methodsUsing pan Notch inhibitors and newly developed human antibodies that specifically neutralize Notch receptor 1 activation, we investigated a role for Notch signaling in GM-CSF-primed transmigration of human blood eosinophils in vitro and in the airway accumulation of mouse eosinophils in vivo.
resultsNotch receptor 1 was constitutively active in freshly isolated human blood eosinophils, and inhibition of Notch signaling or specific blockade of Notch receptor 1 activation during GM-CSF priming impaired priming-enhanced eosinophil transendothelial migration in vitro. Inclusion of Notch signaling inhibitors during priming was associated with diminished ERK phosphorylation, and ERK-MAPK activation was required for GM-CSF priming-induced transmigration. In vivo in mice, eosinophil accumulation within allergic airways was impaired following systemic treatment with Notch inhibitor, or adoptive transfer of eosinophils treated ex vivo with Notch inhibitor.
conclusionsThese data identify Notch signaling as an intrinsic pathway central to GM-CSF priming-induced eosinophil tissue migration.
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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.