Evidence map›Paper›PMID 31077130›Full record

ArticleBMC microbiology2019

Ectromelia virus suppresses expression of cathepsins and cystatins in conventional dendritic cells to efficiently execute the replication process.

Magdalena Bossowska-Nowicka, Matylda B Mielcarska, Marta Romaniewicz, Monika M Kaczmarek, Karolina P Gregorczyk-Zboroch, Justyna Struzik, Marta Grodzik, Małgorzata M Gieryńska, Felix N Toka, Lidia Szulc-Dąbrowska

Open access · goldAbstract read
In one paragraph

Article in BMC microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. The Key Role of Lysosomal Protease Cathepsins in Viral Infections.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Review
  8. Article
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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

10 authors at 2 institutions in 2 countries.

Magdalena Bossowska-NowickaDivision of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences - SGGW, Ciszewskiego 8, 02-786, Warsaw, Poland.
Matylda B MielcarskaDivision of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences - SGGW, Ciszewskiego 8, 02-786, Warsaw, Poland.
Marta RomaniewiczMolecular Biology Laboratory, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland.
Monika M KaczmarekMolecular Biology Laboratory, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland.
Karolina P Gregorczyk-ZborochDivision of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences - SGGW, Ciszewskiego 8, 02-786, Warsaw, Poland.
Justyna StruzikDivision of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences - SGGW, Ciszewskiego 8, 02-786, Warsaw, Poland.
Marta GrodzikDivision of Nanobiotechnology, Department of Animal Nutrition and Biotechnology, Faculty of Animal Sciences, Warsaw University of Life Sciences-SGGW, Warsaw, Poland.
Małgorzata M GieryńskaDivision of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences - SGGW, Ciszewskiego 8, 02-786, Warsaw, Poland.
Felix N TokaDivision of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences - SGGW, Ciszewskiego 8, 02-786, Warsaw, Poland.
Lidia Szulc-DąbrowskaDivision of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences - SGGW, Ciszewskiego 8, 02-786, Warsaw, Poland. lidia_szulc@sggw.pl.ORCID 0000-0002-5436-6556
Warsaw University of Life Sciences · PLInLife Institute of Animal Reproduction and Food Research, Polish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCathepsins are a group of endosomal proteases present in many cells including dendritic cells (DCs). The activity of cathepsins is regulated by their endogenous inhibitors - cystatins. Cathepsins are crucial to antigen processing during viral and bacterial infections, and as such are a prerequisite to antigen presentation in the context of major histocompatibility complex class I and II molecules. Due to the involvement of DCs in both innate and adaptive immune responses, and the quest to understand the impact of poxvirus infection on host cells, we investigated the influence of ectromelia virus (ECTV) infection on cathepsin and cystatin levels in murine conventional DCs (cDCs). ECTV is a poxvirus that has evolved many mechanisms to avoid host immune response and is able to replicate productively in DCs.

resultsOur results showed that ECTV-infection of JAWS II DCs and primary murine GM-CSF-derived bone marrow cells down-regulated both mRNA and protein of cathepsin B, L and S, and cystatin B and C, particularly during the later stages of infection. Moreover, the activity of cathepsin B, L and S was confirmed to be diminished especially at later stages of infection in JAWS II cells. Consequently, ECTV-infected DCs had diminished ability to endocytose and process a soluble antigen. Close examination of cellular protein distribution showed that beginning from early stages of infection, the remnants of cathepsin L and cystatin B co-localized and partially co-localized with viral replication centers (viral factories), respectively. Moreover, viral yield increased in cDCs treated with siRNA against cathepsin B, L or S and subsequently infected with ECTV.

conclusionsTaken together, our results indicate that infection of cDCs with ECTV suppresses cathepsins and cystatins, and alters their cellular distribution which impairs the cDC function. We propose this as an additional viral strategy to escape immune responses, enabling the virus to replicate effectively in infected cells.

Indexed as

AnimalsCathepsinsCystatinsDendritic CellsDown-RegulationEctromelia virusEndosomesGene Knockdown TechniquesMaleMiceMice, Inbred C57BLRNA, Small InterferingVirus ReplicationCathepsinsCystatinsRNA, Small InterferingCathepsinsCystatinsDendritic cellsECTV

Identifiers

PMID31077130
PMCPMC6509786
OpenAlexW2947604697

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.