Evidence map›Paper›PMID 20029461›Full record

ArticleCellular & molecular immunology2010

Intracellular signaling mechanisms regulating the activation of human eosinophils by the novel Th2 cytokine IL-33: implications for allergic inflammation.

Joyce Y S Chow, Chun K Wong, Phyllis F Y Cheung, Christopher W K Lam

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 93 citations in OpenAlex.

  1. Matrix stiffness induces endothelial network senescence.bioRxiv : the preprint server for biology · 2025
    Article
  2. Tartrate-Resistant Acid Phosphatase 5 (TRAP5) Promotes Eosinophil Migration During Allergic Asthma.American journal of respiratory cell and molecular biology · 2025
    Article
  3. Development and dysfunction of structural cells in eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2024
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. TSLP, IL-33, and IL-25: Not just for allergy and helminth infection.The Journal of allergy and clinical immunology · 2022
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Interleukin-33 and ST2 Signaling in Tumor Microenvironment.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2019
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Joyce Y S ChowDepartment of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.
Chun K Wong
Phyllis F Y Cheung
Christopher W K Lam
Prince of Wales Hospital · CNChinese University of Hong Kong · CNMacau University of Science and Technology · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The novel interleukin (IL)-1 family cytokine IL-33 has been shown to activate T helper 2 (Th2) lymphocytes, mast cells and basophils to produce an array of proinflammatory cytokines, as well as to mediate blood eosinophilia, IgE secretion and hypertrophy of airway epithelium in mice. In the present study, we characterized the activation of human eosinophils by IL-33, and investigated the underlying intracellular signaling mechanisms. IL-33 markedly enhanced eosinophil survival and upregulated cell surface expression of the adhesion molecule intercellular adhesion molecule (ICAM)-1 on eosinophils, but it suppressed that of ICAM-3 and L-selectin. In addition, IL-33 mediates significant release of the proinflammatory cytokine IL-6 and the chemokines CXCL8 and CCL2. We found that IL-33-mediated enhancement of survival, induction of adhesion molecules, and release of cytokines and chemokines were differentially regulated by activation of the nuclear factor (NF)-kappaB, p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) pathways. Furthermore, we compared the above IL-33 activities with two structurally and functionally related cytokines, IL-1beta and IL-18. IL-1beta, but not IL-18, markedly upregulated cell surface expression of ICAM-1. IL-1beta and IL-18 also significantly enhanced eosinophil survival, and induced the release of IL-6 and chemokines CXCL8 and CCL2 via the activation of the NF-kappaB, p38 MAPK and ERK pathways. Synergistic effects on the release of IL-6 were also observed in combined treatment with IL-1beta, IL-18 and IL-33. Taken together, our findings provide insight into IL-33-mediated activation of eosinophils via differential intracellular signaling cascades in the immunopathogenesis of allergic inflammation.

Indexed as

MAP Kinase Signaling SystemCell Adhesion MoleculesCells, CulturedCell SurvivalEosinophilsHumansHypersensitivityI-kappa B KinaseInterleukin-18Interleukin-1betaInterleukin-33InterleukinsIntracellular Spacep38 Mitogen-Activated Protein KinasesTh2 CellsCell Adhesion MoleculesI-kappa B KinaseIL33 protein, humanInterleukin-18Interleukin-1betaInterleukin-33Interleukinsp38 Mitogen-Activated Protein Kinases

Identifiers

PMID20029461
PMCPMC4003257
OpenAlexW2061420419

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.