Evidence map›Paper›PMID 30042333›Full record

ReviewInternational journal of molecular sciences2018

Interleukin-1 Beta-A Friend or Foe in Malignancies?

Rebekka Bent, Lorna Moll, Stephan Grabbe, Matthias Bros

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 262 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
262citing papers in PubMed, 5 pooled it
12.4field-weighted citation impact, top 1% 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

262 citing papers in PubMed, 5 syntheses or guidelines pooled it, 428 citations in OpenAlex.

  1. Interaction of HIF-1a with various cell death pathways in tumor immune microenvironment (TIME).Apoptosis : an international journal on programmed cell death · 2026
    Pooled it
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  6. Trial
  7. Review
  8. Interleukin-1β Gene (Current oncology (Toronto, Ont.) · 2026
    Article
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  10. Review
  11. Observational
  12. Article
  13. Review
  14. Article
  15. Pyroptosis: Turning Up the Heat on Cancer.Annual review of immunology · 2026
    Review
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  17. Article
  18. Review
  19. Review
  20. Review

202 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

4 authors at 2 institutions in 1 country.

Rebekka BentDepartment of Dermatology, University Medical Center, 55131 Mainz, Germany. Rebekka.Bent@unimedizin-mainz.de.
Lorna MollDepartment of Dermatology, University Medical Center, 55131 Mainz, Germany. Lorna.Moll@unimedizin-mainz.de.
Stephan GrabbeDepartment of Dermatology, University Medical Center, 55131 Mainz, Germany. Stephan.Grabbe@unimedizin-mainz.de.
Matthias BrosDepartment of Dermatology, University Medical Center, 55131 Mainz, Germany. mbros@uni-mainz.de.
University Medical Center of the Johannes Gutenberg University Mainz · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-1 beta (IL-1β) is induced by inflammatory signals in a broad number of immune cell types. IL-1β (and IL-18) are the only cytokines which are processed by caspase-1 after inflammasome-mediated activation. This review aims to summarize current knowledge about parameters of regulation of IL-1β expression and its multi-facetted role in pathophysiological conditions. IL-1 signaling activates innate immune cells including antigen presenting cells, and drives polarization of CD4+ T cells towards T helper type (Th) 1 and Th17 cells. Therefore, IL-1β has been attributed a largely beneficial role in resolving acute inflammations, and by initiating adaptive anti-tumor responses. However, IL-1β generated in the course of chronic inflammation supports tumor development. Furthermore, IL-1β generated within the tumor microenvironment predominantly by tumor-infiltrating macrophages promotes tumor growth and metastasis via different mechanisms. These include the expression of IL-1 targets which promote neoangiogenesis and of soluble mediators in cancer-associated fibroblasts that evoke antiapoptotic signaling in tumor cells. Moreover, IL-1 promotes the propagation of myeloid-derived suppressor cells. Using genetic mouse models as well as agents for pharmacological inhibition of IL-1 signaling therapeutically applied for treatment of IL-1 associated autoimmune diseases indicate that IL-1β is a driver of tumor induction and development.

Indexed as

Adaptive ImmunityAnimalsAntineoplastic AgentsCytokinesHumansImmunity, InnateInflammasomesInflammationInterleukin-1betaMacrophagesMiceModels, AnimalNeoplasmsAntineoplastic AgentsCytokinesInflammasomesInterleukin-1betainflammasomeinterleukin-1βmyeloid-derived suppressor cellpromotertumortumor-associated macrophage

Identifiers

PMID30042333
PMCPMC6121377
OpenAlexW2883276763

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.