Evidence map›Paper›PMID 29875777›Full record

ArticleFrontiers in immunology2018

Blockade of MIF-CD74 Signalling on Macrophages and Dendritic Cells Restores the Antitumour Immune Response Against Metastatic Melanoma.

Carlos R Figueiredo, Ricardo A Azevedo, Sasha Mousdell, Pedro T Resende-Lara, Lucy Ireland, Almudena Santos, Natalia Girola, Rodrigo L O R Cunha, Michael C Schmid, Luciano Polonelli and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

123 citing papers in PubMed, 189 citations in OpenAlex.

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  18. Cellular Landscape of Synovial Chondromatosis Synovium Revealed by Single-Cell RNA Sequencing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  19. Article
  20. Single-Cell RNA Sequencing of Ewing Sarcoma Tumors Demonstrates Transcriptional Heterogeneity and Clonal Evolution.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article

63 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

12 authors at 4 institutions in 4 countries.

Carlos R FigueiredoDepartment of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.
Ricardo A AzevedoExperimental Oncology Unit (UNONEX), Department of Microbiology, Immunology and Parasitology, Federal University of São Paulo (UNIFESP), São Paulo, Brazil.
Sasha MousdellDepartment of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.
Pedro T Resende-LaraLaboratory of Computational Biology and Bioinformatics, Federal University of ABC, Santo André, Brazil.
Lucy IrelandDepartment of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.
Almudena SantosDepartment of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.
Natalia GirolaExperimental Oncology Unit (UNONEX), Department of Microbiology, Immunology and Parasitology, Federal University of São Paulo (UNIFESP), São Paulo, Brazil.
Rodrigo L O R CunhaChemical Biology Laboratory, Natural and Human Sciences Center, Federal University of ABC, Santo André, Brazil.
Michael C SchmidDepartment of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.
Luciano PolonelliUnit of Biomedical, Biotechnological and Translational Sciences, Department of Medicine and Surgery, Universitá degli Studi di Parma, Parma, Italy.
Luiz R TravassosExperimental Oncology Unit (UNONEX), Department of Microbiology, Immunology and Parasitology, Federal University of São Paulo (UNIFESP), São Paulo, Brazil.
Ainhoa MielgoDepartment of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.
University of Liverpool · GBUniversidade Federal de São Paulo · BRUniversidade Federal do ABC · BRUniversity of Parma · IT

Funding

Medical Research Council MR/P018920/1Wellcome TrustWellcome Trust 102521/Z/13/Z
6 · The paper itself

Abstract

Mounting an effective immune response against cancer requires the activation of innate and adaptive immune cells. Metastatic melanoma is the most aggressive form of skin cancer. While immunotherapies have shown a remarkable success in melanoma treatment, patients develop resistance by mechanisms that include the establishment of an immune suppressive tumor microenvironment. Thus, understanding how metastatic melanoma cells suppress the immune system is vital to develop effective immunotherapies against this disease. In this study, we find that macrophages (MOs) and dendritic cells (DCs) are suppressed in metastatic melanoma and that the Ig-CDR-based peptide C36L1 is able to restore MOs and DCs' antitumorigenic and immunogenic functions and to inhibit metastatic growth in lungs. Specifically, C36L1 treatment is able to repolarize M2-like immunosuppressive MOs into M1-like antitumorigenic MOs, and increase the number of immunogenic DCs, and activated cytotoxic T cells, while reducing the number of regulatory T cells and monocytic myeloid-derived suppressor cells in metastatic lungs. Mechanistically, we find that C36L1 directly binds to the MIF receptor CD74 which is expressed on MOs and DCs, disturbing CD74 structural dynamics and inhibiting MIF signaling on these cells. Interfering with MIF-CD74 signaling on MOs and DCs leads to a decrease in the expression of immunosuppressive factors from MOs and an increase in the capacity of DCs to activate cytotoxic T cells. Our findings suggest that interfering with MIF-CD74 immunosuppressive signaling in MOs and DCs, using peptide-based immunotherapy can restore the antitumor immune response in metastatic melanoma. Our study provides the rationale for further development of peptide-based therapies to restore the antitumor immune response in metastatic melanoma.

Indexed as

ImmunitySignal TransductionAnimalsAntigens, Differentiation, B-LymphocyteDendritic CellsHistocompatibility Antigens Class IIMacrophage Migration-Inhibitory FactorsMacrophagesMaleMelanomaMelanoma, ExperimentalMiceModels, BiologicalModels, MolecularNeoplasm MetastasisPeptidesAntigens, Differentiation, B-LymphocyteHistocompatibility Antigens Class IIinvariant chainmacrophage migration inhibitory factor receptorMacrophage Migration-Inhibitory FactorsPeptidesReceptors, ImmunologicCD74dendritic cellsimmune responsemacrophage migration inhibitory factormacrophagesmetastatic melanomapeptide-based immunotherapy

Identifiers

PMID29875777
PMCPMC5974174
OpenAlexW2800769338

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.