Evidence map›Paper›PMID 24752321›Full record

ArticlePloS one2014

Trypanosoma cruzi infection down-modulates the immunoproteasome biosynthesis and the MHC class I cell surface expression in HeLa cells.

Ricardo Camargo, Liliam O Faria, Alexander Kloss, Cecília B F Favali, Ulrike Kuckelkorn, Peter-Michael Kloetzel, Cezar Martins de Sá, Beatriz D Lima

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

9 citing papers in PubMed, 22 citations in OpenAlex.

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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

8 authors at 2 institutions in 2 countries.

Ricardo CamargoDepartamento de Biologia Celular, Universidade de Brasília, Campus Universitário Darcy Ribeiro, Brasília, Distrito Federal, Brazil.
Liliam O FariaDepartamento de Biologia Celular, Universidade de Brasília, Campus Universitário Darcy Ribeiro, Brasília, Distrito Federal, Brazil.
Alexander KlossInstitute für Biochimie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Cecília B F FavaliDepartamento de Biologia Celular, Universidade de Brasília, Campus Universitário Darcy Ribeiro, Brasília, Distrito Federal, Brazil.
Ulrike KuckelkornInstitute für Biochimie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Peter-Michael KloetzelInstitute für Biochimie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Cezar Martins de SáDepartamento de Biologia Celular, Universidade de Brasília, Campus Universitário Darcy Ribeiro, Brasília, Distrito Federal, Brazil.
Beatriz D LimaDepartamento de Biologia Celular, Universidade de Brasília, Campus Universitário Darcy Ribeiro, Brasília, Distrito Federal, Brazil.
Universidade de Brasília · BRCharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Generally, Trypanosoma cruzi infection in human is persistent and tends to chronicity, suggesting that the parasite evade the immune surveillance by down regulating the intracellular antigen processing routes. Within the MHC class I pathway, the majority of antigenic peptides are generated by the proteasome. However, upon IFN-γ stimulation, the catalytic constitutive subunits of the proteasome are replaced by the subunits β1i/LMP2, β2i/MECL-1 and β5i/LMP7 to form the immunoproteasome. In this scenario, we analyzed whether the expression and activity of the constitutive and the immunoproteasome as well as the expression of other components of the MHC class I pathway are altered during the infection of HeLa cells with T. cruzi. By RT-PCR and two-dimensional gel electrophoresis analysis, we showed that the expression and composition of the constitutive proteasome is not affected by the parasite. In contrast, the biosynthesis of the β1i, β2i, β5i immunosubunits, PA28β, TAP1 and the MHC class I molecule as well as the proteasomal proteolytic activities were down-regulated in infected-IFN-γ-treated cell cultures. Taken together, our results provide evidence that the protozoan T. cruzi specifically modulates its infection through an unknown posttranscriptional mechanism that inhibits the expression of the MHC class I pathway components.

Indexed as

Chagas DiseaseGenes, MHC Class IHeLa CellsHumansImmunoprecipitationInterferon-gammaProteasome Endopeptidase ComplexReverse Transcriptase Polymerase Chain ReactionTrypanosoma cruziInterferon-gammaProteasome Endopeptidase Complex

Identifiers

PMID24752321
PMCPMC3994161
OpenAlexW2084192209

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.