Evidence map›Paper›PMID 26922618›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2016

Interleukin-33 in tumorigenesis, tumor immune evasion, and cancer immunotherapy.

Binfeng Lu, Min Yang, Qingqing Wang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 2% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Integrated Transcriptomic Analysis ofInternational journal of molecular sciences · 2026
    Article
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  4. Article
  5. Article
  6. Review
  7. Inflammatory factors collaboratively linkFrontiers in immunology · 2025
    Review
  8. Review
  9. Article
  10. Innate Immune Cells in Melanoma: Implications for Immunotherapy.International journal of molecular sciences · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Amphiregulin couples IL1RL1Science advances · 2023
    Article
  15. Review
  16. AllergoOncology: Role of immune cells and immune proteins.Clinical and translational allergy · 2022
    Review
  17. Review
  18. Review
  19. Article
  20. Review

9 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 2 countries.

Binfeng LuDepartment of Immunology, University of Pittsburgh School of Medicine, 200 Lothrop Street, Pittsburgh, PA, 15261, USA. binfeng@pitt.edu.
Min YangDepartment of Immunology, Institute of Medical Biotechnology, School of Biology and Basic Medical Sciences, Soochow University, Suzhou, People's Republic of China.
Qingqing WangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Soochow University · CNUniversity of Pittsburgh · USZhejiang University · CN

Funding

RPCI-UPCI Ovarian Cancer SPOREP50CA159981 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MOYSICH, KIRSTEN B. · 2013 to 2025
$19.6M
Cellular and molecular mechanisms underlying IL-33-mediated anti-tumor immunityR21CA167229 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LU, BINFENG · 2013 to 2014
$360k
NCI NIH HHS P50 CA159981NCI NIH HHS R21 CA167229
6 · The paper itself

Abstract

Interleukin-33 (IL-33) is a member of the IL-1 gene family and mainly expressed in the nucleus of tissue lining cells, stromal cells, and activated myeloid cells. IL-33 is considered a damage-associated molecular pattern (DAMP) molecule and plays an important role in many physiological and pathological settings such as tissue repair, allergy, autoimmune disease, infectious disease, and cancer. The biological functions of IL-33 include maintaining tissue homeostasis, enhancing type 1 and 2 cellular immune responses, and mediating fibrosis during chronic inflammation. IL-33 exerts diverse functions through signaling via its receptor ST2, which is expressed in many types of cells including regulatory T cells (Treg), group 2 innate lymphoid cells (ILC2s), myeloid cells, cytotoxic NK cells, Th2 cells, Th1 cells, and CD8(+) T cells. Tumor development results in downregulation of IL-33 in epithelial cells but upregulation of IL-33 in the tumor stroma and serum. The current data suggest that IL-33 expression in tumor cells increases immunogenicity and promotes type 1 antitumor immune responses through CD8(+) T cells and NK cells, whereas IL-33 in tumor stroma and serum facilitates immune suppression via Treg and myeloid-derived suppressor cell (MDSC). Understanding the role of IL-33 in cancer immunobiology sheds lights on targeting this cytokine for cancer immunotherapy.

Indexed as

AnimalsCancer-Associated FibroblastsCell Transformation, NeoplasticFibrosisHumansImmunity, InnateImmunologic SurveillanceImmunotherapyInflammationInterleukin-33Myeloid CellsNeoplasm MetastasisNeoplasmsT-Lymphocyte SubsetsTumor EscapeInterleukin-33Cancer immunotherapyCD8 T cellInterleukin-33MDSCTumorigenesis

Identifiers

PMID26922618
OpenAlexW2283478476

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.