Evidence map›Paper›PMID 23526630›Full record

ArticleEuropean journal of immunology2013

Complement opsonization of HIV-1 results in a different intracellular processing pattern and enhanced MHC class I presentation by dendritic cells.

Veronica Tjomsland, Rada Ellegård, Adam Burgener, Kenzie Mogk, Karlhans F Che, Garrett Westmacott, Jorma Hinkula, Jeffrey D Lifson, Marie Larsson

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2013. 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
1.1field-weighted citation impact, top 26% 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, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. The role of the complement system in HIV infection and preeclampsia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. 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

9 authors at 4 institutions in 3 countries.

Veronica TjomslandDivision of Molecular Virology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Rada Ellegård
Adam Burgener
Kenzie Mogk
Karlhans F Che
Garrett Westmacott
Jorma Hinkula
Jeffrey D Lifson
Marie Larsson
Linköping University · SEUniversity of Manitoba · CACanadian Science Centre for Human and Animal Health · CAFrederick National Laboratory for Cancer Research · US

Funding

Innate NKT Cells in HIV InfectionR37AI052731 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NIXON, DOUGLAS F · 2007 to 2016
$3.1M
Innate NKT Cells in HIV InfectionR01AI052731 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NIXON, DOUGLAS F · 2002 to 2006
$2.1M
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001ENIAID NIH HHS R01 AI052731NIAID NIH HHS R37 AI052731
6 · The paper itself

Abstract

Induction of optimal HIV-1-specific T-cell responses, which can contribute to controlling viral infection in vivo, depends on antigen processing and presentation processes occurring in DCs. Opsonization can influence the routing of antigen processing and pathways used for presentation. We studied antigen proteolysis and the role of endocytic receptors in MHC class I (MHCI) and II (MHCII) presentation of antigens derived from HIV-1 in human monocyte-derived immature DCs (IDCs) and mature DCs, comparing free and complement opsonized HIV-1 particles. Opsonization of virions promoted MHCI presentation by DCs, indicating that complement opsonization routes more virions toward the MHCI presentation pathway. Blockade of macrophage mannose receptor (MMR) and β7-integrin enhanced MHCI and MHCII presentation by IDCs and mature DCs, whereas the block of complement receptor 3 decreased MHCI and MHCII presentation. In addition, we found that IDC and MDC proteolytic activities were modulated by HIV-1 exposure; complement-opsonized HIV-1 induced an increased proteasome activity in IDCs. Taken together, these findings indicate that endocytic receptors such as MMR, complement receptor 3, and β7-integrin can promote or disfavor antigen presentation probably by routing HIV-1 into different endosomal compartments with distinct efficiencies for degradation of viral antigens and MHCI and MHCII presentation, and that HIV-1 affects the antigen-processing machinery.

Indexed as

Antibodies, BlockingAntigen PresentationAntigens, ViralCD8-Positive T-LymphocytesCell DifferentiationCells, CulturedComplement System ProteinsDendritic CellsEndocytosisHistocompatibility Antigens Class IHIV-1HIV InfectionsHumansIntegrin beta ChainsLectins, C-TypeLymphocyte ActivationAntibodies, BlockingAntigens, ViralComplement System ProteinsHistocompatibility Antigens Class Iintegrin beta7Integrin beta ChainsLectins, C-TypeMannose-Binding LectinsMannose ReceptorReceptors, Cell SurfaceReceptors, Complement

Identifiers

PMID23526630
PMCPMC3738931
OpenAlexW1950676599

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.