Evidence map›Paper›PMID 23071666›Full record

ArticlePloS one2012

IRF1 and NF-kB restore MHC class I-restricted tumor antigen processing and presentation to cytotoxic T cells in aggressive neuroblastoma.

Silvia Lorenzi, Matteo Forloni, Loredana Cifaldi, Chiara Antonucci, Arianna Citti, Renata Boldrini, Marco Pezzullo, Aurora Castellano, Vincenzo Russo, Pierre van der Bruggen and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

61 citing papers in PubMed, 90 citations in OpenAlex.

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  15. Bridging the divide: unveiling mutual immunological pathways of cancer and pregnancy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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1 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

13 authors at 5 institutions in 3 countries.

Silvia LorenziPaediatric Haematology/Oncology Department, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Matteo Forloni
Loredana Cifaldi
Chiara Antonucci
Arianna Citti
Renata Boldrini
Marco Pezzullo
Aurora Castellano
Vincenzo Russo
Pierre van der Bruggen
Patrizio Giacomini
Franco Locatelli
Doriana Fruci
Boston Children's Hospital · USBambino Gesù Children's Hospital · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITThe San Raffaele Telethon Institute for Gene Therapy · ITUCLouvain · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroblastoma (NB), the most common solid extracranial cancer of childhood, displays a remarkable low expression of Major Histocompatibility Complex class I (MHC-I) and Antigen Processing Machinery (APM) molecules, including Endoplasmic Reticulum (ER) Aminopeptidases, and poorly presents tumor antigens to Cytotoxic T Lymphocytes (CTL). We have previously shown that this is due to low expression of the transcription factor NF-kB p65. Herein, we show that not only NF-kB p65, but also the Interferon Regulatory Factor 1 (IRF1) and certain APM components are low in a subset of NB cell lines with aggressive features. Whereas single transfection with either IRF1, or NF-kB p65 is ineffective, co-transfection results in strong synergy and substantial reversion of the MHC-I/APM-low phenotype in all NB cell lines tested. Accordingly, linked immunohistochemistry expression patterns between nuclear IRF1 and p65 on the one hand, and MHC-I on the other hand, were observed in vivo. Absence and presence of the three molecules neatly segregated between high-grade and low-grade NB, respectively. Finally, APM reconstitution by double IRF1/p65 transfection rendered a NB cell line susceptible to killing by anti MAGE-A3 CTLs, lytic efficiency comparable to those seen upon IFN-γ treatment. This is the first demonstration that a complex immune escape phenotype can be rescued by reconstitution of a limited number of master regulatory genes. These findings provide molecular insight into defective MHC-I expression in NB cells and provide the rational for T cell-based immunotherapy in NB variants refractory to conventional therapy.

Indexed as

Antigen PresentationAntigensAntigens, NeoplasmBlotting, WesternCell Line, TumorHistocompatibility Antigens Class IHumansImmunohistochemistryInterferon-gammaInterferon Regulatory Factor-1Jurkat CellsNeoplasm ProteinsNeuroblastomaReverse Transcriptase Polymerase Chain ReactionRNA InterferenceT-Lymphocytes, CytotoxicAntigensAntigens, NeoplasmHistocompatibility Antigens Class IInterferon-gammaInterferon Regulatory Factor-1IRF1 protein, humanMAGEA3 protein, humanNeoplasm ProteinsTranscription Factor RelA

Identifiers

PMID23071666
PMCPMC3465322
OpenAlexW2007105300

What OpenQuestion holds

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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.