ArticleBlood2015
Eosinophil-specific deletion of IκBα in mice reveals a critical role of NF-κB-induced Bcl-xL for inhibition of apoptosis.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Eosinophils and eosinophil-associated diseases: An update.The Journal of allergy and clinical immunology · 2018Pooled it
- Eosinophil biology in COPD: from scientific insight to clinical treatment action.ERJ open research · 2026Review
- Rediscovering eosinophil identity through tissue adaptation.Nature immunology · 2026Review
- IL-25 Enhances Eosinophil-Associated Inflammation in Angiostrongylus cantonensis-Infected Mice.Parasite immunology · 2026Article
- The Role of and Therapeutic Strategies for Eosinophils in Atopic Dermatitis.Biomedicines · 2026Review
- Crosstalk between inflammation and autophagy in CeD organoids.Scientific reports · 2026Article
- Pro-inflammatory and counter-regulatory modulators of interleukin-5-driven eosinophil programs: a framework for precision medicine in eosinophilic diseases.Frontiers in immunology · 2026Review
- Regulation of eosinophil recruitment and heterogeneity during allergic airway inflammation.Frontiers in allergy · 2025Review
- Review
- 4-Octyl Itaconate Alleviates Airway Eosinophilic Inflammation by Suppressing Chemokines and Eosinophil Development.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Article
- Pre-Protection and Mechanism of Crude Extracts fromAnimals : an open access journal from MDPI · 2023Article
- Lentinan improves intestinal inflammation and gut dysbiosis in antibiotics-induced mice.Scientific reports · 2022Article
- Eosinophilic inflammation: An Appealing Target for Pharmacologic Treatments in Severe Asthma.Biomedicines · 2022Review
- The aryl hydrocarbon receptor contributes to tissue adaptation of intestinal eosinophils in mice.The Journal of experimental medicine · 2022Article
- OX40 Expression in Eosinophils Aggravates OVA-Induced Eosinophilic Gastroenteritis.Frontiers in immunology · 2022Article
- The Interactions Between Autoinflammation and Type 2 Immunity: From Mechanistic Studies to Epidemiologic Associations.Frontiers in immunology · 2022Review
- Clonally expanded, GPR15-expressing pathogenic effector TScience immunology · 2021Article
- Emerging Evidence for Pleiotropism of Eosinophils.International journal of molecular sciences · 2021Review
- Physiology and pathology of eosinophils: Recent developments: Summary of the Focus Workshop Organized by DGAKI.Scandinavian journal of immunology · 2021Review
Corrections and comments
- Commented on by
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Eosinophils are associated with type 2 immune responses to allergens and helminths. They release various proinflammatory mediators and toxic proteins on activation and are therefore considered proinflammatory effector cells. Eosinophilia is promoted by the cytokines interleukin (IL)-3, IL-5, and granulocyte macrophage-colony-stimulating factor (GM-CSF) and can result from enhanced de novo production or reduced apoptosis. In this study, we show that only IL-5 induces differentiation of eosinophils from bone marrow precursors, whereas IL-5, GM-CSF, and to a lesser extent IL-3 promote survival of mature eosinophils. The receptors for these cytokines use the common β chain, which serves as the main signaling unit linked to signal transducer and activator of transcription 5, p38 mitogen-activated protein kinase, and nuclear factor (NF)-κB pathways. Inhibition of NF-κB induced apoptosis of in vitro cultured eosinophils. Selective deletion of IκBα in vivo resulted in enhanced expression of Bcl-xL and reduced apoptosis during helminth infection. Retroviral overexpression of Bcl-xL promoted survival, whereas pharmacologic inhibition of Bcl-xL in murine or human eosinophils induced rapid apoptosis. These results suggest that therapeutic strategies targeting Bcl-xL in eosinophils could improve health conditions in allergic inflammatory diseases.
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.