Evidence map›Paper›PMID 30873154›Full record

ArticleFrontiers in immunology2019

Iron and Ferritin Modulate MHC Class I Expression and NK Cell Recognition.

Rosa Sottile, Giorgia Federico, Cinzia Garofalo, Rossana Tallerico, Maria Concetta Faniello, Barbara Quaresima, Costanza Maria Cristiani, Maddalena Di Sanzo, Gianni Cuda, Valeria Ventura and 9 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 61 citations in OpenAlex.

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  15. Ferritinophagy induced ferroptosis in the management of cancer.Cellular oncology (Dordrecht, Netherlands) · 2024
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  16. Amelioration of nephrotoxicity by targeting ferroptosis: role of NCOA4, IREB2, and SLC7a11 signaling.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
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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

19 authors at 4 institutions in 3 countries.

Rosa SottileTumor Immunology and Immunopathology Laboratory, Department of Experimental and Clinical Medicine, University Magna Graecia of Catanzaro, Catanzaro, Italy.
Giorgia FedericoDepartment of Molecular Medicine and Medical Biotechnologies Federico II University, Naples, Italy.
Cinzia GarofaloTumor Immunology and Immunopathology Laboratory, Department of Experimental and Clinical Medicine, University Magna Graecia of Catanzaro, Catanzaro, Italy.
Rossana TallericoTumor Immunology and Immunopathology Laboratory, Department of Experimental and Clinical Medicine, University Magna Graecia of Catanzaro, Catanzaro, Italy.
Maria Concetta FanielloResearch Center of Advanced Biochemistry and Molecular Biology, Department of Experimental and Clinical Medicine, Magna Græcia University of Catanzaro, Catanzaro, Italy.
Barbara QuaresimaResearch Center of Advanced Biochemistry and Molecular Biology, Department of Experimental and Clinical Medicine, Magna Græcia University of Catanzaro, Catanzaro, Italy.
Costanza Maria CristianiTumor Immunology and Immunopathology Laboratory, Department of Experimental and Clinical Medicine, University Magna Graecia of Catanzaro, Catanzaro, Italy.
Maddalena Di SanzoResearch Center of Advanced Biochemistry and Molecular Biology, Department of Experimental and Clinical Medicine, Magna Græcia University of Catanzaro, Catanzaro, Italy.
Gianni CudaLaboratory of Proteomics, Research Center of Advanced Biochemistry and Molecular Biology, Department of Experimental and Clinical Medicine, Magna Græcia University of Catanzaro, Catanzaro, Italy.
Valeria VenturaTumor Immunology and Immunopathology Laboratory, Department of Experimental and Clinical Medicine, University Magna Graecia of Catanzaro, Catanzaro, Italy.
Arnika Kathleen WagnerDepartment of Microbiology, Cell and Tumor Biology (MTC), Karolinska Institutet, Stockholm, Sweden.
Gianluca ContròDepartment of Health Sciences, University of Catanzaro Magna Graecia, Catanzaro, Italy.
Nicola PerrottiDepartment of Health Sciences, University of Catanzaro Magna Graecia, Catanzaro, Italy.
Elio GullettaDivision of Clinical Pathology, Department of Health Sciences, Magna Graecia University, Catanzaro, Italy.
Soldano FerroneDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States.
Klas KärreDepartment of Microbiology, Cell and Tumor Biology (MTC), Karolinska Institutet, Stockholm, Sweden.
Francesco Saverio CostanzoResearch Center of Advanced Biochemistry and Molecular Biology, Department of Experimental and Clinical Medicine, Magna Græcia University of Catanzaro, Catanzaro, Italy.
Francesca CarlomagnoDepartment of Molecular Medicine and Medical Biotechnologies Federico II University, Naples, Italy.
Ennio CarboneTumor Immunology and Immunopathology Laboratory, Department of Experimental and Clinical Medicine, University Magna Graecia of Catanzaro, Catanzaro, Italy.
Magna Graecia University · ITKarolinska Institutet · SEFederico II University Hospital · ITHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability of pathogens to sequester iron from their host cells and proteins affects their virulence. Moreover, iron is required for various innate host defense mechanisms as well as for acquired immune responses. Therefore, intracellular iron concentration may influence the interplay between pathogens and immune system. Here, we investigated whether changes in iron concentrations and intracellular ferritin heavy chain (FTH) abundance may modulate the expression of Major Histocompatibility Complex molecules (MHC), and susceptibility to Natural Killer (NK) cell cytotoxicity. FTH downregulation, either by shRNA transfection or iron chelation, led to MHC surface reduction in primary cancer cells and macrophages. On the contrary, mouse embryonic fibroblasts (MEFs) from NCOA4 null mice accumulated FTH for ferritinophagy impairment and displayed MHC class I cell surface overexpression. Low iron concentration, but not FTH, interfered with IFN-γ receptor signaling, preventing the increase of MHC-class I molecules on the membrane by obstructing STAT1 phosphorylation and nuclear translocation. Finally, iron depletion and FTH downregulation increased the target susceptibility of both primary cancer cells and macrophages to NK cell recognition. In conclusion, the reduction of iron and FTH may influence the expression of MHC class I molecules leading to NK cells activation.

Indexed as

AnimalsApoferritinsCell Line, TumorCells, CulturedCytotoxicity, ImmunologicDeferoxamineEmbryo, MammalianFibroblastsGene ExpressionHeLa CellsHistocompatibility Antigens Class IHumansInterferon-gammaIronK562 CellsKiller Cells, NaturalApoferritinsDeferoxamineHistocompatibility Antigens Class IInterferon-gammaIronNcoA4 protein, mouseNuclear Receptor CoactivatorsSiderophoresHLAIFNγironMHC-INK cellsSTAT1

Identifiers

PMID30873154
PMCPMC6404638
OpenAlexW2916290398

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.