Evidence map›Paper›PMID 26177543›Full record

ArticlePloS one2015

The Human Autoantibody Response to Apolipoprotein A-I Is Focused on the C-Terminal Helix: A New Rationale for Diagnosis and Treatment of Cardiovascular Disease?

Sabrina Pagano, Hubert Gaertner, Fabrice Cerini, Tiphaine Mannic, Nathalie Satta, Priscila Camillo Teixeira, Paul Cutler, François Mach, Nicolas Vuilleumier, Oliver Hartley

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-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

17 citing papers in PubMed, 29 citations in OpenAlex.

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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 4 institutions in 1 country.

Sabrina PaganoDepartment of Human Protein Sciences, Faculty of Medicine, University of Geneva, Geneva, Switzerland; Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Geneva, Switzerland.
Hubert GaertnerDepartment of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Fabrice CeriniDepartment of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Tiphaine MannicDepartment of Human Protein Sciences, Faculty of Medicine, University of Geneva, Geneva, Switzerland; Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Geneva, Switzerland.
Nathalie SattaDepartment of Human Protein Sciences, Faculty of Medicine, University of Geneva, Geneva, Switzerland; Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Geneva, Switzerland.
Priscila Camillo TeixeiraPharmaceutical Sciences, Pharma Research and Early Development, F.Hoffmann-La Roche, Basel, Switzerland.
Paul CutlerPharmaceutical Sciences, Pharma Research and Early Development, F.Hoffmann-La Roche, Basel, Switzerland.
François MachDivision of Cardiology, Foundation for Medical Researches, University of Geneva, Geneva, Switzerland.
Nicolas VuilleumierDepartment of Human Protein Sciences, Faculty of Medicine, University of Geneva, Geneva, Switzerland; Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Geneva, Switzerland.
Oliver HartleyDepartment of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
University of Geneva · CHRoche (Switzerland) · CHUniversity Hospital of Geneva · CHFoundation for laboratory medicine · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiovascular disease (CVD) is the leading cause of death worldwide and new approaches for both diagnosis and treatment are required. Autoantibodies directed against apolipoprotein A-I (ApoA-I) represent promising biomarkers for use in risk stratification of CVD and may also play a direct role in pathogenesis. METHODOLOGY: To characterize the anti-ApoA-I autoantibody response, we measured the immunoreactivity to engineered peptides corresponding to the different alpha-helical regions of ApoA-I, using plasma from acute chest pain cohort patients known to be positive for anti-ApoA-I autoantibodies. PRINCIPAL

findingsOur results indicate that the anti-ApoA-I autoantibody response is strongly biased towards the C-terminal alpha-helix of the protein, with an optimized mimetic peptide corresponding to this part of the protein recapitulating the diagnostic accuracy for an acute ischemic coronary etiology (non-ST segment elevation myocardial infarction and unstable angina) obtainable using intact endogenous ApoA-I in immunoassay. Furthermore, the optimized mimetic peptide strongly inhibits the pathology-associated capacity of anti-ApoA-I antibodies to elicit proinflammatory cytokine release from cultured human macrophages.

conclusionsIn addition to providing a rationale for the development of new approaches for the diagnosis and therapy of CVD, our observations may contribute to the elucidation of how anti-ApoA-I autoantibodies are elicited in individuals without autoimmune disease.

Indexed as

Amino Acid SequenceApolipoprotein A-IAutoantibodiesCardiovascular DiseasesCircular DichroismHumansImmobilized ProteinsImmunoglobulin GInflammation MediatorsInterleukin-6Molecular Sequence DataPeptidesProtein EngineeringProtein Structure, SecondaryTumor Necrosis Factor-alphaAPOA1 protein, humanApolipoprotein A-IAutoantibodiesImmobilized ProteinsImmunoglobulin GInflammation MediatorsInterleukin-6PeptidesTumor Necrosis Factor-alpha

Identifiers

PMID26177543
PMCPMC4503694
OpenAlexW1568776786

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Registered trials

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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.