Evidence map›Paper›PMID 26628365›Full record

ArticleCell reports2015

Multinucleated Giant Cells Are Specialized for Complement-Mediated Phagocytosis and Large Target Destruction.

Ronny Milde, Julia Ritter, Glenys A Tennent, Andrzej Loesch, Fernando O Martinez, Siamon Gordon, Mark B Pepys, Admar Verschoor, Laura Helming

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

85 citing papers in PubMed, 160 citations in OpenAlex.

  1. Article
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  6. Polyploidy and Senescence of Cancer Cells: Impact of Cell Fusion.Advances in experimental medicine and biology · 2026
    Review
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  18. Upregulation of ATP6V0D2 benefits intracellular survival ofFrontiers in cellular and infection microbiology · 2024
    Article
  19. Article
  20. Review

25 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

9 authors at 5 institutions in 2 countries.

Ronny MildeInstitute for Medical Microbiology, Immunology and Hygiene, Technische Universität München, 81675 Munich, Germany.
Julia RitterInstitute for Medical Microbiology, Immunology and Hygiene, Technische Universität München, 81675 Munich, Germany.
Glenys A TennentWolfson Drug Discovery Unit, Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, Royal Free Campus, University College London, London NW3 2PF, UK.
Andrzej LoeschWolfson Drug Discovery Unit, Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, Royal Free Campus, University College London, London NW3 2PF, UK.
Fernando O MartinezKennedy Rheumatology Institute, University of Oxford, Oxford OX3 7LD, UK.
Siamon GordonSir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.
Mark B PepysWolfson Drug Discovery Unit, Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, Royal Free Campus, University College London, London NW3 2PF, UK. Electronic address: m.pepys@ucl.ac.uk.
Admar VerschoorInstitute for Medical Microbiology, Immunology and Hygiene, Technische Universität München, 81675 Munich, Germany; Institute for Systemic Inflammation Research, Universität zu Lübeck, 23538 Lübeck, Germany. Electronic address: admar.verschoor@uksh.de.
Laura HelmingInstitute for Medical Microbiology, Immunology and Hygiene, Technische Universität München, 81675 Munich, Germany.
Institute of Medical Microbiology and Hygiene · DEUniversity College London · GBUniversity of Oxford · GBTechnical University of Munich · DEThe Royal Free Hospital · GB

Funding

Medical Research Council G0901596Medical Research Council G7900510
6 · The paper itself

Abstract

Multinucleated giant cells (MGCs) form by fusion of macrophages and are presumed to contribute to the removal of debris from tissues. In a systematic in vitro analysis, we show that IL-4-induced MGCs phagocytosed large and complement-opsonized materials more effectively than their unfused M2 macrophage precursors. MGC expression of complement receptor 4 (CR4) was increased, but it functioned primarily as an adhesion integrin. In contrast, although expression of CR3 was not increased, it became functionally activated during fusion and was located on the extensive membrane ruffles created by excess plasma membrane arising from macrophage fusion. The combination of increased membrane area and activated CR3 specifically equips MGCs to engulf large complement-coated targets. Moreover, we demonstrate these features in vivo in the recently described complement-dependent therapeutic elimination of systemic amyloid deposits by MGCs. MGCs are evidently more than the sum of their macrophage parts.

Indexed as

AmyloidAnimalsBone Marrow CellsCD11c AntigenCD18 AntigensComplement C3CricetinaeGiant CellsHumansIntegrin alphaXbeta2Interleukin-4Macrophage Colony-Stimulating FactorMacrophagesMiceMice, Inbred C57BLMice, KnockoutAmyloidCD11c AntigenCD18 AntigensComplement C3Integrin alphaXbeta2Interleukin-4Macrophage Colony-Stimulating FactorReceptors, IgGTetradecanoylphorbol Acetate

Identifiers

PMID26628365
PMCPMC4675895
OpenAlexW2180027722

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.