Evidence map›Paper›PMID 27806341›Full record

ArticleOncotarget2016

Exogenous cathepsin G upregulates cell surface MHC class I molecules on immune and glioblastoma cells.

Madleen Giese, Nadine Turiello, Nicole Molenda, David Palesch, Annika Meid, Roman Schroeder, Paola Basilico, Charaf Benarafa, Marc-Eric Halatsch, Michal Zimecki and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

12 citing papers in PubMed, 13 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

13 authors at 3 institutions in 3 countries.

Madleen GieseDepartment of Neurosurgery, Ulm University Medical Center, Ulm, Germany.
Nadine TurielloDepartment of Neurosurgery, Ulm University Medical Center, Ulm, Germany.
Nicole MolendaDepartment of Neurosurgery, Ulm University Medical Center, Ulm, Germany.
David PaleschInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.
Annika MeidDepartment of Neurosurgery, Ulm University Medical Center, Ulm, Germany.
Roman SchroederDepartment of Neurosurgery, Ulm University Medical Center, Ulm, Germany.
Paola BasilicoTheodor Kocher Institute, University of Bern, Bern, Switzerland.
Charaf BenarafaTheodor Kocher Institute, University of Bern, Bern, Switzerland.
Marc-Eric HalatschDepartment of Neurosurgery, Ulm University Medical Center, Ulm, Germany.
Michal ZimeckiLudwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.
Mike-Andrew WesthoffDepartment Pediatrics and Adolescent Medicine, Ulm University Medical Center, Ulm, Germany.
Christian Rainer WirtzDepartment of Neurosurgery, Ulm University Medical Center, Ulm, Germany.
Timo BursterDepartment of Neurosurgery, Ulm University Medical Center, Ulm, Germany.
Universität Ulm · DEUniversity of Bern · CHLudwik Hirszfeld Institute of Immunology and Experimental Therapy · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Major histocompatibility complex (MHC) class I molecules present antigenic peptides to cytotoxic T cells. During an adaptive immune response, MHC molecules are regulated by several mechanisms including lipopolysaccharide (LPS) and interferon gamma (IFN-g). However, it is unclear whether the serine protease cathepsin G (CatG), which is generally secreted by neutrophils at the site of inflammation, might regulate MHC I molecules. We identified CatG, and to a higher extend CatG and lactoferrin (LF), as an exogenous regulator of cell surface MHC I expression of immune cells and glioblastoma stem cells. In addition, levels of MHC I molecules are reduced on dendritic cells from CatG deficient mice compared to their wild type counterparts. Furthermore, cell surface CatG on immune cells, including T cells, B cells, and NK cells triggers MHC I on THP-1 monocytes suggesting a novel mechanism for CatG to facilitate intercellular communication between infiltrating cells and the respective target cell. Subsequently, our findings highlight the pivotal role of CatG as a checkpoint protease which might force target cells to display their intracellular MHC I:antigen repertoire.

Indexed as

AnimalsCathepsin GCell LineCell Line, TumorCell MembraneDisease Models, AnimalFemaleGene Expression Regulation, NeoplasticGlioblastomaHistocompatibility Antigens Class IHumansImmune SystemLactoferrinMaleMiceMice, KnockoutCathepsin GHistocompatibility Antigens Class ILactoferrinCatG deficient micecathepsin Gglioblastoma stem cellsImmune responseImmunityImmunology and Microbiology SectionlactoferrinMHC class I

Identifiers

PMID27806341
PMCPMC5342690
OpenAlexW2542360133

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.