Evidence map›Paper›PMID 37021528›Full record

ArticleHaematologica2023

IL-18 and VEGF-A trigger type 2 innate lymphoid cell accumulation and pro-tumoral function in chronic myeloid leukemia.

Benedetta Fiordi, Valentina Salvestrini, Gabriele Gugliotta, Fausto Castagnetti, Antonio Curti, Daniel E Speiser, Emanuela Marcenaro, Camilla Jandus, Sara Trabanelli

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Haematologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. ILC2s and their immune checkpoints in the antitumor response.Journal for immunotherapy of cancer · 2026
    Review
  3. IL-18-Mediated Tumor Immune Evasion.Current issues in molecular biology · 2026
    Review
  4. PGI2 restricts trained ILC2 responses in allergic inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Article
  5. Article
  6. Article
  7. 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

9 authors at 4 institutions in 2 countries.

Benedetta FiordiDepartment of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland; Ludwig Institute for Cancer Research, Lausanne Branch, Lausanne, Switzerland.
Valentina SalvestriniIRCCS Azienda Ospedaliero-Universitaria di Bologna, Institute of Hematology « Seràgnoli », Bologna, Italy.
Gabriele GugliottaIRCCS Azienda Ospedaliero-Universitaria di Bologna, Institute of Hematology « Seràgnoli », Bologna, Italy.
Fausto CastagnettiIRCCS Azienda Ospedaliero-Universitaria di Bologna, Institute of Hematology « Seràgnoli », Bologna, Italy.
Antonio CurtiIRCCS Azienda Ospedaliero-Universitaria di Bologna, Institute of Hematology « Seràgnoli », Bologna, Italy.
Daniel E SpeiserDepartment of Oncology, Lausanne University Hospital (CHUV) and University of Lausanne, Epalinges, Switzerland.
Emanuela MarcenaroDepartment of Experimental Medicine (DIMES), University of Genova, Genova, Italy; IRCCS Ospedale Policlinico San Martino, Genova, Italy.
Camilla JandusDepartment of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland; Ludwig Institute for Cancer Research, Lausanne Branch, Lausanne, Switzerland.
Sara TrabanelliDepartment of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland; Ludwig Institute for Cancer Research, Lausanne Branch, Lausanne, Switzerland. sara.trabanelli@unige.ch.
University of Geneva · CHLudwig Cancer Research · CHUniversity of Genoa · ITUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is a hematologic malignancy associated to an unregulated growth of myeloid cells in bone marrow (BM) and peripheral blood (PB), characterized by the BCR-ABL1 translocation. Given the known cytokine impairment in the leukemic niche of CML, we investigated the impact of this microenvironmental dysregulation on innate lymphoid cells (ILC), whose role in cancer has recently emerged. Three ILC subsets are identified based on transcriptional profiles and cytokine secretion. We observed that interleukin 18 (IL-18) and vascular endothelial growth factor A (VEGF-A) are increased in CML patients' sera and that ILC2 are enriched in CML PB and BM. We found that IL-18 drives ILC2 proliferation and that CML ILC2 highly express CXCR4 and CXCR7 BM-homing receptors, potentially explaining their enrichment in PB and BM, respectively. Next, we showed that ILC2 are hyper-activated through a tumor-derived VEGF-Adependent mechanism, which leads to higher IL-13 secretion. In response to IL-13, leukemic cells increase their clonogenic capacity. Finally, we discovered that the pro-tumoral axis involving VEGF-A, IL-18 and ILC2 was disrupted upon tyrosine kinase inhibitor treatment, normalizing the levels of all these players in CML patients responding to therapy. Overall, our study uncovers the involvement of ILC2 in CML progression, mediated by VEGF-A and IL-18.

Indexed as

Leukemia, Myelogenous, Chronic, BCR-ABL PositiveVascular Endothelial Growth Factor AFusion Proteins, bcr-ablHumansImmunity, InnateInterleukin-13Interleukin-18LymphocytesFusion Proteins, bcr-ablInterleukin-13Interleukin-18Vascular Endothelial Growth Factor A

Identifiers

PMID37021528
PMCPMC10483352
OpenAlexW4362657822

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.