Evidence map›Paper›PMID 31964554›Full record

ReviewVaccine2020

Opportunities for an atherosclerosis vaccine: From mice to humans.

Payel Roy, Amal J Ali, Kouji Kobiyama, Yanal Ghosheh, Klaus Ley

Open access · greenAbstract readReview
In one paragraph

Review in Vaccine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Anti-Atherogenic Mechanisms and Therapies.Current atherosclerosis reports · 2025
    Review
  4. Article
  5. A bibliometric analysis of vaccination against atherosclerosis.Human vaccines & immunotherapeutics · 2024
    Article
  6. Review
  7. Review
  8. Inflammation and Atherosclerosis: Prospects for Clinical Trials.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Role of the adaptive immune system in atherosclerosis.Biochemical Society transactions · 2020
    Review
  18. T cell subsets and functions in atherosclerosis.Nature reviews. Cardiology · 2020
    Review
  19. Review
  20. 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

5 authors at 2 institutions in 2 countries.

Payel RoyDivision of Inflammation Biology, La Jolla Institute for Immunology, 9420, Athena Circle Drive, La Jolla, CA 92037, USA.
Amal J AliDivision of Inflammation Biology, La Jolla Institute for Immunology, 9420, Athena Circle Drive, La Jolla, CA 92037, USA.
Kouji KobiyamaDivision of Inflammation Biology, La Jolla Institute for Immunology, 9420, Athena Circle Drive, La Jolla, CA 92037, USA; Division of Vaccine Science, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
Yanal GhoshehDivision of Inflammation Biology, La Jolla Institute for Immunology, 9420, Athena Circle Drive, La Jolla, CA 92037, USA.
Klaus LeyDivision of Inflammation Biology, La Jolla Institute for Immunology, 9420, Athena Circle Drive, La Jolla, CA 92037, USA; Department of Bioengineering, University of California San Diego, 9500 Gilman Drive, MC0412, La Jolla, CA 92093, USA. Electronic address: klaus@lji.org.
La Jolla Institute for Immunology · USUniversity of California, San Diego · US

Funding

Project 4: APOB-specific CD4 and CD8 T cells exacerbate atherosclerosisP01HL136275 · NHLBI · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI Catherine C Hedrick · 2017 to 2026
$25.5M
Vascular macrophages and T cells in atherosclerosisR35HL145241 · NHLBI · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI LEY, KLAUS F. · 2019 to 2025
$5.9M
NHLBI NIH HHS P01 HL136275NHLBI NIH HHS R35 HL145241
6 · The paper itself

Abstract

Atherosclerosis, the major underlying cause of cardiovascular diseases (CVD), is the number one killer globally. The disease pathogenesis involves a complex interplay between metabolic and immune components. Although lipid-lowering drugs such as statins curb the risks associated with CVD, significant residual inflammatory risk remains. Substantial evidence from experimental models and clinical studies has established the role of inflammation and immune effector mechanisms in the pathogenesis of atherosclerosis. Several stages of the disease are affected by host-mediated antigen-specific adaptive immune responses that play either protective or proatherogenic roles. Therefore, strategies to boost an anti-atherogenic humoral and T regulatory cell response are emerging as preventative or therapeutic strategies to lowering inflammatory residual risks. Vaccination holds promise as an efficient, durable and relatively inexpensive approach to induce protective adaptive immunity in atherosclerotic patients. In this review, we discuss the status and opportunities for a human atherosclerosis vaccine. We describe (1) some of the immunomodulatory therapeutic interventions tested in atherosclerosis (2) the immune targets identified in pre-clinical and clinical investigations (3) immunization strategies evaluated in animal models (4) past and ongoing clinical trials to examine the safety and efficacy of human atherosclerosis vaccines and (5) strategies to improve and optimize vaccination in humans (antigen selection, formulation, dose and delivery).

Indexed as

AtherosclerosisVaccinesAdaptive ImmunityAnimalsHumansInflammationMiceVaccinationVaccinesAntigen-specificAtherosclerosisImmunomodulationPeptide-based vaccineTregs

Identifiers

PMID31964554
PMCPMC7939143
OpenAlexW3000686494

What OpenQuestion holds

Textmetadata
LicenceTDM
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.