ArticleJournal of immunology (Baltimore, Md. : 1950)2015
IL-3 Maintains Activation of the p90S6K/RPS6 Pathway and Increases Translation in Human Eosinophils.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 41 citations in OpenAlex.
- Identification of STAT3 signaling as a shared pathogenic signature in systemic lupus erythematosus, chronic obstructive pulmonary disease, and asthma.Scientific reports · 2025Article
- A motif in the 5'untranslated region of messenger RNAs regulates protein synthesis in a S6 kinase-dependent manner.Advances in biological regulation · 2023Article
- Article
- Article
- IL-3-Induced Immediate Expression of c-Cells · 2022Article
- An open microfluidic coculture model of fibroblasts and eosinophils to investigate mechanisms of airway inflammation.Frontiers in bioengineering and biotechnology · 2022Article
- Review
- Increased IL-6 and Potential IL-6 trans-signalling in the airways after an allergen challenge.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2021Article
- Siglec-8 Signals Through a Non-Canonical Pathway to Cause Human Eosinophil DeathFrontiers in immunology · 2021Article
- Infectious Complications of Biological and Small Molecule Targeted Immunomodulatory Therapies.Clinical microbiology reviews · 2020Review
- Eosinophil cytolysis on Immunoglobulin G is associated with microtubule formation and suppression of rho-associated protein kinase signalling.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2020Article
- The Cellular Functions of Eosinophils: Collegium Internationale Allergologicum (CIA) Update 2020.International archives of allergy and immunology · 2020Review
- Innate Immune Modulation by GM-CSF and IL-3 in Health and Disease.International journal of molecular sciences · 2019Review
- Reuse of public, genome-wide, murine eosinophil expression data for hypotheses development.Journal of leukocyte biology · 2018Article
- Proteomic and Phosphoproteomic Changes Induced by Prolonged Activation of Human Eosinophils with IL-3.Journal of proteome research · 2018Article
- Control of cytokine-driven eosinophil migratory behavior by TGF-beta-induced protein (TGFBI) and periostin.PloS one · 2018Article
- RNA-sequencing analysis of lung primary fibroblast response to eosinophil-degranulation products predicts downstream effects on inflammation, tissue remodeling and lipid metabolism.Respiratory research · 2017Article
- Pathological manifestations in lymphatic filariasis correlate with lack of inhibitory properties of IgG4 antibodies on IgE-activated granulocytes.PLoS neglected tropical diseases · 2017Article
- IL-3 up-regulates and activates human eosinophil CD32 and αMβ2 integrin causing degranulation.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2017Article
- The neglected of eosinophil biology, IL-3 finds sustenance in the basophil.Journal of leukocyte biology · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
IL-5 is a major therapeutic target to reduce eosinophilia. However, all of the eosinophil-activating cytokines, such as IL-5, IL-3, and GM-CSF, are typically present in atopic diseases, including allergic asthma. As a result of the functional redundancy of these three cytokines on eosinophils and the loss of IL-5R on airway eosinophils, it is important to take IL-3 and GM-CSF into account to efficiently reduce tissue eosinophil functions. Moreover, these three cytokines signal through a common β-chain receptor but yet differentially affect protein production in eosinophils. Notably, the increased ability of IL-3 to induce the production of proteins, such as semaphorin-7A, without affecting mRNA levels suggests a unique influence of IL-3 on translation. The purpose of this study was to identify the mechanisms by which IL-3 distinctively affects eosinophil function compared with IL-5 and GM-CSF, with a focus on protein translation. Peripheral blood eosinophils were used to study intracellular signaling and protein translation in cells activated with IL-3, GM-CSF, or IL-5. We establish that, unlike GM-CSF or IL-5, IL-3 triggers prolonged signaling through activation of ribosomal protein S6 (RPS6) and the upstream kinase 90-kDa ribosomal S6 kinase (p90S6K). Blockade of p90S6K activation inhibited phosphorylation of RPS6 and IL-3-enhanced semaphorin-7A translation. Furthermore, in an allergen-challenged environment, in vivo phosphorylation of RPS6 and p90S6K was enhanced in human airway compared with circulating eosinophils. Our findings provide new insights into the mechanisms underlying differential activation of eosinophils by IL-3, GM-CSF, and IL-5. These observations identify IL-3 and its downstream intracellular signals as novel targets that should be considered to modulate eosinophil functions.
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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.