Evidence map›Paper›PMID 22238605›Full record

ArticlePloS one2012

Depletion of B2 but not B1a B cells in BAFF receptor-deficient ApoE mice attenuates atherosclerosis by potently ameliorating arterial inflammation.

Tin Kyaw, Christopher Tay, Hamid Hosseini, Peter Kanellakis, Tahlia Gadowski, Fabeinne MacKay, Peter Tipping, Alex Bobik, Ban-Hock Toh

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02428374 (Role of Innate and Adaptive Immunity After Acute Myocardial Infarction BATTLE-AMI Study), which is not on this map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
7.5field-weighted citation impact, top 2% 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.

NCT02428374 phase4unknown statusstarted 2015, after this paper: background citation

Role of Innate and Adaptive Immunity After Acute Myocardial Infarction BATTLE-AMI Study (B And T Types of Lymphocytes Evaluation in Acute Myocardial Infarction)

Ran2015Enrolled300Registered outcomes30Posted comparisons0ConditionsMyocardial FibrosisArmsRosuvastatin plus clopidogrel, Rosuvastatin plus ticagrelor, Simvastatin plus clopidogrel, Simvastatin plus ticagrelor
Open the trial in the graph
3 · Its place in the literature

Who cites it

89 citing papers in PubMed, 176 citations in OpenAlex.

  1. Article
  2. Inflammation and Immune Mechanisms in Atherosclerosis.Reviews in cardiovascular medicine · 2026
    Review
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  7. Article
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  14. Article
  15. Tipping the Scale: Atheroprotective IgM-Producing B Cells in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  16. Review
  17. Review
  18. Review
  19. B cells and atherosclerosis: A HIV perspective.Journal of cellular physiology · 2024
    Review
  20. Review

29 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Tin KyawVascular Biology and Atherosclerosis Laboratory, Baker IDI Heart and Diabetes Institute, Victoria, Australia. Tinsoe.Kyaw@bakeridi.edu.au
Christopher Tay
Hamid Hosseini
Peter Kanellakis
Tahlia Gadowski
Fabeinne MacKay
Peter Tipping
Alex Bobik
Ban-Hock Toh
Baker Heart and Diabetes Institute · AUMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have recently identified conventional B2 cells as atherogenic and B1a cells as atheroprotective in hypercholesterolemic ApoE(-/-) mice. Here, we examined the development of atherosclerosis in BAFF-R deficient ApoE(-/-) mice because B2 cells but not B1a cells are selectively depleted in BAFF-R deficient mice. We fed BAFF-R(-/-) ApoE(-/-) (BaffR.ApoE DKO) and BAFF-R(+/+)ApoE(-/-) (ApoE KO) mice a high fat diet (HFD) for 8-weeks. B2 cells were significantly reduced by 82%, 81%, 94%, 72% in blood, peritoneal fluid, spleen and peripheral lymph nodes respectively; while B1a cells and non-B lymphocytes were unaffected. Aortic atherosclerotic lesions assessed by oil red-O stained-lipid accumulation and CD68+ macrophage accumulation were decreased by 44% and 50% respectively. B cells were absent in atherosclerotic lesions of BaffR.ApoE DKO mice as were IgG1 and IgG2a immunoglobulins produced by B2 cells, despite low but measurable numbers of B2 cells and IgG1 and IgG2a immunoglobulin concentrations in plasma. Plasma IgM and IgM deposits in atherosclerotic lesions were also reduced. BAFF-R deficiency in ApoE(-/-) mice was also associated with a reduced expression of VCAM-1 and fewer macrophages, dendritic cells, CD4+ and CD8+ T cell infiltrates and PCNA+ cells in lesions. The expression of proinflammatory cytokines, TNF-α, IL1-β and proinflammatory chemokine MCP-1 was also reduced. Body weight and plasma cholesterols were unaffected in BaffR.ApoE DKO mice. Our data indicate that B2 cells are important contributors to the development of atherosclerosis and that targeting the BAFF-R to specifically reduce atherogenic B2 cell numbers while preserving atheroprotective B1a cell numbers may be a potential therapeutic strategy to reduce atherosclerosis by potently reducing arterial inflammation.

Indexed as

AnimalsApolipoproteins EArteriesArteritisAtherosclerosisB-Cell Activation Factor ReceptorChemokine CCL2CytokinesCytoprotectionDown-RegulationEndothelial CellsGene Expression RegulationInflammation MediatorsMaleMiceMice, Inbred C57BLApolipoproteins EB-Cell Activation Factor ReceptorCcl2 protein, mouseChemokine CCL2CytokinesInflammation MediatorsTnfrsf13c protein, mouse

Identifiers

PMID22238605
PMCPMC3251583
OpenAlexW2061781448

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.