Evidence map›Paper›PMID 30779113›Full record

ArticleEuropean journal of immunology2019

Poly(I:C) stimulation is superior than Imiquimod to induce the antitumoral functional profile of tumor-conditioned macrophages.

Akihiro Maeda, Elisabeth Digifico, Fernando T Andon, Alberto Mantovani, Paola Allavena

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
  6. Designing nucleic acid-based therapeutics for cancer treatment: Updates on the state of the art.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Review
  7. Article
  8. Emerging immunologic approaches as cancer anti-angiogenic therapies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Tumor-Associated Macrophage Subsets: Shaping Polarization and Targeting.International journal of molecular sciences · 2023
    Review
  14. Review
  15. Breast cancer associated CD169Frontiers in immunology · 2023
    Article
  16. Review
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  18. Article
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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

5 authors at 1 institution in 1 country.

Akihiro MaedaHumanitas Clinical and Research Center IRCCS, Department of Innate Immunity and Inflammation, via Manzoni 56, 20089, Rozzano, Milan, Italy.ORCID 0000-0003-4797-0314
Elisabeth DigificoHumanitas University, Via A. Manzoni 113, 20089, Rozzano, Milan, Italy.
Fernando T AndonHumanitas Clinical and Research Center IRCCS, Department of Innate Immunity and Inflammation, via Manzoni 56, 20089, Rozzano, Milan, Italy.
Alberto MantovaniHumanitas Clinical and Research Center IRCCS, Department of Innate Immunity and Inflammation, via Manzoni 56, 20089, Rozzano, Milan, Italy.
Paola AllavenaHumanitas Clinical and Research Center IRCCS, Department of Innate Immunity and Inflammation, via Manzoni 56, 20089, Rozzano, Milan, Italy.
Humanitas University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage plasticity is the ability of mononuclear phagocytes to change phenotype, function, and genetic reprogramming upon encounter of specific local stimuli. In the tumor microenvironment, Tumor-Associated Macrophages (TAMs) acquire an immune-suppressive and tumor-promoting phenotype. With the aim to re-educate TAMs to antitumor effectors, in this study, we used two immunestimulatory compounds: the TLR7 agonist Imiquimod (IMQ) and the TLR3 agonist Poly(I:C). To better mimic in vitro the response of TAMs, we used Tumor-Conditioned Macrophages (TC-Mϕ) differentiated in the presence of tumor cell supernatants. Our results show that TC-Mϕ respond differently from conventional M2-polarized macrophages. Upon stimulation with IMQ, TC-Mϕ did not upregulate major histocompatibility complex (MHC II) molecules and unexpectedly expressed increased CD206. With both compounds, TC-Mϕ produced higher levels of inflammatory cytokines than M2 macrophages. IMQ and Poly(I:C) differed in the types of regulated genes and secreted mediators. Reflecting their signaling pathways, only IMQ significantly induced IL-1β and IL-6, while only Poly(I:C) stimulated CXCL10, and both upregulated CCL5. Of note, using a novel cytotoxicity assay, Poly(I:C), but not IMQ, was effective in triggering the cytotoxic activity of TC-Mϕ against cancer cells. Overall, the results demonstrate that Poly(I:C) stimulation of TC-Mϕ is superior than IMQ in terms of macrophage re-education toward antitumor effectors.

Indexed as

Antineoplastic AgentsCell Line, TumorCell MembraneCytokinesHumansImiquimodImmunomodulationMacrophagesNeoplasmsPoly I-CTumor MicroenvironmentAntineoplastic AgentsCytokinesImiquimodPoly I-CImiquimodImmunomodulationImmunotherapyPoly(I:C)Tumor-associated macrophages (TAMs)

Identifiers

PMID30779113
PMCPMC6563448
OpenAlexW2917517401

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.