Evidence map›Paper›PMID 31757993›Full record

ArticleScientific reports2019

Induction of HLA-A2 restricted CD8 T cell responses against ApoB100 peptides does not affect atherosclerosis in a humanized mouse model.

Frank H Schaftenaar, Jacob Amersfoort, Hidde Douna, Mara J Kröner, Amanda C Foks, Ilze Bot, Bram A Slütter, Gijs H M van Puijvelde, Jan W Drijfhout, Johan Kuiper

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. CD8Nature reviews. Cardiology · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. CD8Cells · 2020
    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

10 authors at 2 institutions in 1 country.

Frank H SchaftenaarDivision of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden, The Netherlands. f.h.schaftenaar@lacdr.leidenuniv.nl.
Jacob AmersfoortDivision of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden, The Netherlands.
Hidde DounaDivision of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden, The Netherlands.
Mara J KrönerDivision of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden, The Netherlands.
Amanda C FoksDivision of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden, The Netherlands.
Ilze BotDivision of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden, The Netherlands.ORCID http://orcid.org/0000-0002-1242-1959
Bram A SlütterDivision of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden, The Netherlands.
Gijs H M van PuijveldeDivision of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden, The Netherlands.
Jan W DrijfhoutDepartment of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands.
Johan KuiperDivision of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden, The Netherlands. j.kuiper@lacdr.leidenuniv.nl.
Centre for Human Drug Research · NLLeiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular diseases form the most common cause of death worldwide, with atherosclerosis as main etiology. Atherosclerosis is marked by cholesterol rich lipoprotein deposition in the artery wall, evoking a pathogenic immune response. Characteristic for the disease is the pathogenic accumulation of macrophages in the atherosclerotic lesion, which become foam cells after ingestion of large quantities of lipoproteins. We hypothesized that, by inducing a CD8 T cell response towards lipoprotein derived apolipoprotein-B100 (ApoB100), lesional macrophages, that are likely to cross-present lipoprotein constituents, can specifically be eliminated. Based on in silico models for protein processing and MHC-I binding, 6 putative CD8 T cell epitopes derived from ApoB100 were synthesized. HLA-A2 binding was confirmed for all peptides by T2 cell binding assays and recall responses after vaccination with the peptides proved that 5 of 6 peptides could induce CD8 T cell responses. Induction of ApoB100 specific CD8 T cells did not impact plaque size and cellular composition in HLA-A2 and human ApoB100 transgenic LDLr

Indexed as

AnimalsAntibodies, Monoclonal, HumanizedApolipoprotein B-100AtherosclerosisCD8-Positive T-LymphocytesCells, CulturedDisease Models, AnimalEpitopes, T-LymphocyteHLA-A2 AntigenHumansLymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicPeptidesReceptors, LDLAntibodies, Monoclonal, HumanizedApolipoprotein B-100Epitopes, T-LymphocyteHLA-A2 AntigenLDLR protein, humanPeptidesReceptors, LDL

Identifiers

PMID31757993
PMCPMC6874568
OpenAlexW2990082316

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.