Evidence map›Paper›PMID 30260027›Full record

ArticleJournal of cellular biochemistry2019

Gene expression in chronic granulomatous disease and interferon-γ receptor-deficient cells treated in vitro with interferon-γ.

Josias B Frazão, Martino Colombo, Cedric Simillion, Adem Bilican, Irene Keller, Daniel Wüthrich, Zhiqing Zhu, Michal J Okoniewski, Rémy Bruggmann, Antonio Condino-Neto and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.1field-weighted citation impact, top 53% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. 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

11 authors at 4 institutions in 3 countries.

Josias B FrazãoDepartment of Immunology, Institutes of Biomedical Sciences and Tropical Medicine, University of São Paulo, São Paulo, Brazil.
Martino ColomboInterfaculty Bioinformatics Unit, Swiss Institute of Bioinformatics, University of Bern, Bern, Switzerland.
Cedric SimillionInterfaculty Bioinformatics Unit, Swiss Institute of Bioinformatics, University of Bern, Bern, Switzerland.
Adem BilicanInterfaculty Bioinformatics Unit, Swiss Institute of Bioinformatics, University of Bern, Bern, Switzerland.
Irene KellerInterfaculty Bioinformatics Unit, Swiss Institute of Bioinformatics, University of Bern, Bern, Switzerland.
Daniel WüthrichInterfaculty Bioinformatics Unit, Swiss Institute of Bioinformatics, University of Bern, Bern, Switzerland.
Zhiqing ZhuDepartment of Pediatrics, University of Massachusetts Medical School, Worcester, Massachusetts.
Michal J OkoniewskiScientific IT Services, Swiss Federal Institute of Technology, Zurich, Switzerland.
Rémy BruggmannInterfaculty Bioinformatics Unit, Swiss Institute of Bioinformatics, University of Bern, Bern, Switzerland.
Antonio Condino-NetoDepartment of Immunology, Institutes of Biomedical Sciences and Tropical Medicine, University of São Paulo, São Paulo, Brazil.
Peter E NewburgerDepartment of Pediatrics, University of Massachusetts Medical School, Worcester, Massachusetts.ORCID 0000-0002-8615-673X
University of Bern · CHUniversity of Massachusetts Chan Medical School · USÉcole Polytechnique Fédérale de Lausanne · CHUniversidade de São Paulo · BR

Funding

Engineered Cas9 Nucleases with Single-Genomic-Site Precision for CYBB CorrectionR01GM115911 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SONTHEIMER, ERIK J., WOLFE, SCOT A · 2016 to 2019
$1.6M
NIGMS NIH HHS R01 GM115911
6 · The paper itself

Abstract

Interferon-γ (IFN-γ) plays an important role in innate and adaptive immunity against intracellular infections and is used clinically for the prevention and control of infections in chronic granulomatous disease (CGD) and inborn defects in the IFN-γ/interleukin (IL)-12 axis. Using transcriptome profiling (RNA-seq), we sought to identify differentially expressed genes, transcripts and exons in Epstein-Barr virus-transformed B lymphocytes (B-EBV) cells from CGD patients, IFN-γ receptor deficiency patients, and normal controls, treated in vitro with IFN-γ for 48 hours. Our results show that IFN-γ increased the expression of a diverse array of genes related to different cellular programs. In cells from normal controls and CGD patients, IFN-γ-induced expression of genes relevant to oxidative killing, nitric oxide synthase pathway, proteasome-mediated degradation, antigen presentation, chemoattraction, and cell adhesion. IFN-γ also upregulated genes involved in diverse stages of messenger RNA (mRNA) processing including pre-mRNA splicing, as well as others implicated in the folding, transport, and assembly of proteins. In particular, differential exon expression of WARS (encoding tryptophanyl-transfer RNA synthetase, which has an essential function in protein synthesis) induced by IFN-γ in normal and CGD cells suggests that this gene may have an important contribution to the benefits of IFN-γ treatment for CGD. Upregulation of mRNA and protein processing related genes in CGD and IFNRD cells could mediate some of the effects of IFN-γ treatment. These data support the concept that IFN-γ treatment may contribute to increased immune responses against pathogens through regulation of genes important for mRNA and protein processing.

Indexed as

B-LymphocytesCell LineExonsGene ExpressionGranulomatous Disease, ChronicHerpesvirus 4, HumanHumansInterferon-gammaInterferon gamma ReceptorReceptors, InterferonRNA, MessengerRNA-SeqRNA SplicingSignal TransductionTryptophan-tRNA LigaseInterferon-gammaInterferon gamma ReceptorReceptors, InterferonRNA, MessengerTryptophan-tRNA LigaseWARS1 protein, humanchronic granulomatous diseaseinterferon-γinterferon-γ receptor deficiencyphagocytetranscriptome

Identifiers

PMID30260027
PMCPMC6336507
OpenAlexW2892660368

What OpenQuestion holds

Textmetadata
LicenceTDM
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.