Evidence map›Paper›PMID 40210642›Full record

ArticleNature communications2025

Hyperinflammatory repolarisation of ovarian cancer patient macrophages by anti-tumour IgE antibody, MOv18, restricts an immunosuppressive macrophage:Treg cell interaction.

Gabriel Osborn, Jacobo López-Abente, Rebecca Adams, Roman Laddach, Melanie Grandits, Heather J Bax, Jitesh Chauhan, Giulia Pellizzari, Mano Nakamura, Chara Stavraka and 18 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. AllergoOncology in Review: Harnessing Allergy in the Field of Oncology to Improve Patient Outcomes.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026
    Review
  6. Article
  7. Review
  8. Regulatory B Cells in Tumor Microenvironment.Current issues in molecular biology · 2026
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
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

28 authors.

Gabriel OsbornSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.
Jacobo López-AbenteSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.
Rebecca AdamsSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.
Roman LaddachSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.
Melanie GranditsSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.
Heather J BaxSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.ORCID http://orcid.org/0000-0003-0432-4160
Jitesh ChauhanSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.
Giulia PellizzariSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.ORCID http://orcid.org/0000-0003-0387-1912
Mano NakamuraSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.
Chara StavrakaSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.ORCID http://orcid.org/0000-0001-7623-299X
Alicia ChenowethSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.
Lais C G F PalharesSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.
Theodore EvanSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.
Jessica Hui Cheah LimCancer Centre at Guy's, Guy's and St Thomas' NHS Foundation Trust, London, UK.
Amanda GrossSeromYx Systems, Inc, Woburn, MA, USA.
Lenny MoiseSeromYx Systems, Inc, Woburn, MA, USA.ORCID http://orcid.org/0000-0002-4410-865X
Shashi JatianiSeromYx Systems, Inc, Woburn, MA, USA.ORCID http://orcid.org/0000-0003-0724-6583
Mariangela FiginiANP2, Department of Advanced Diagnostics, Fondazione IRCCS, Istituto Nazionale dei Tumori, Milan, Italy.ORCID http://orcid.org/0000-0001-9001-8754
Rodolfo BianchiniComparative Medicine, The Interuniversity Messerli Research Institute, University of Veterinary Medicine Vienna, Medical University of Vienna, University of Vienna, Vienna, Austria.ORCID http://orcid.org/0000-0003-0351-6937
Erika Jensen-JarolimComparative Medicine, The Interuniversity Messerli Research Institute, University of Veterinary Medicine Vienna, Medical University of Vienna, University of Vienna, Vienna, Austria.
Sharmistha GhoshCancer Centre at Guy's, Guy's and St Thomas' NHS Foundation Trust, London, UK.
Ana MontesCancer Centre at Guy's, Guy's and St Thomas' NHS Foundation Trust, London, UK.
Ahmad SayasnehCancer Centre at Guy's, Guy's and St Thomas' NHS Foundation Trust, London, UK.
Rebecca KristeleitSchool of Cancer & Pharmaceutical Sciences, King's College London, Guy's Hospital, London, UK.ORCID http://orcid.org/0000-0003-3825-1326
Sophia TsokaDepartment of Informatics, Faculty of Natural, Mathematical and Engineering Sciences, King's College London, Bush House, London, UK.
James SpicerSchool of Cancer & Pharmaceutical Sciences, King's College London, Guy's Hospital, London, UK.ORCID http://orcid.org/0000-0003-3732-8491
Debra H JosephsSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK.
Sophia N KaragiannisSt. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, Guy's Hospital, London, UK. sophia.karagiannis@kcl.ac.uk.ORCID http://orcid.org/0000-0002-4100-7810

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer is the most lethal gynaecological cancer and treatment options remain limited. In a recent first-in-class Phase I trial, the monoclonal IgE antibody MOv18, specific for the tumour-associated antigen Folate Receptor-α, was well-tolerated and preliminary anti-tumoural activity observed. Pre-clinical studies identified macrophages as mediators of tumour restriction and pro-inflammatory activation by IgE. However, the mechanisms of IgE-mediated modulation of macrophages and downstream tumour immunity in human cancer remain unclear. Here we study macrophages from patients with epithelial ovarian cancers naive to IgE therapy. High-dimensional flow cytometry and RNA-seq demonstrate immunosuppressive, FcεR-expressing macrophage phenotypes. Ex vivo co-cultures and RNA-seq interaction analyses reveal immunosuppressive associations between patient-derived macrophages and regulatory T (Treg) cells. MOv18 IgE-engaged patient-derived macrophages undergo pro-inflammatory repolarisation ex vivo and display induction of a hyperinflammatory, T cell-stimulatory subset. IgE reverses macrophage-promoted Treg cell induction to increase CD8+ T cell expansion, a signature associated with improved patient prognosis. On-treatment tumours from the MOv18 IgE Phase I trial show evidence of this IgE-driven immune signature, with increased CD68+ and CD3+ cell infiltration. We demonstrate that IgE induces hyperinflammatory repolarised states of patient-derived macrophages to inhibit Treg cell immunosuppression. These processes may collectively promote immune activation in ovarian cancer patients receiving IgE therapy.

Indexed as

Carcinoma, Ovarian EpithelialImmunoglobulin EMacrophagesOvarian NeoplasmsT-Lymphocytes, RegulatoryCD8-Positive T-LymphocytesFemaleFolate Receptor 1HumansInflammationMiddle AgedReceptors, IgEFolate Receptor 1Immunoglobulin EReceptors, IgE

Identifiers

PMID40210642
PMCPMC11985905

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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.