Evidence map›Paper›PMID 24797388›Full record

ArticlePloS one2014

A novel antibody against human properdin inhibits the alternative complement system and specifically detects properdin from blood samples.

Diana Pauly, Benedikt M Nagel, Jörg Reinders, Tobias Killian, Matthias Wulf, Susanne Ackermann, Boris Ehrenstein, Peter F Zipfel, Christine Skerka, Bernhard H F Weber

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Complement Inhibition in Kidney Transplantation: Where Are We Now?BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023
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  6. A Narrative Review on C3 Glomerulopathy: A Rare Renal Disease.International journal of molecular sciences · 2020
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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.

Diana PaulyInstitute of Human Genetics, University of Regensburg, Regensburg, Germany.
Benedikt M NagelInstitute of Human Genetics, University of Regensburg, Regensburg, Germany.
Jörg ReindersInstitute of Functional Genomics, University of Regensburg, Regensburg, Germany.
Tobias KillianInstitute of Human Genetics, University of Regensburg, Regensburg, Germany.
Matthias WulfInstitute of Human Genetics, University of Regensburg, Regensburg, Germany.
Susanne AckermannDepartment of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, Jena, Germany.
Boris EhrensteinKlinik und Poliklinik für Rheumatologie und Klinische Immunologie, Asklepios Klinikum Bad Abbach, Bad Abbach, Germany.
Peter F ZipfelDepartment of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, Jena, Germany; Department of Infection Biology, Friedrich Schiller University, Jena, Germany.
Christine SkerkaDepartment of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, Jena, Germany.
Bernhard H F WeberInstitute of Human Genetics, University of Regensburg, Regensburg, Germany.
University of Regensburg · DELeibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) · DEAsklepios Kliniken Bad Abbach · DEFriedrich Schiller University Jena · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complement system is an essential part of the innate immune system by acting as a first line of defense which is stabilized by properdin, the sole known positive regulator of the alternative complement pathway. Dysregulation of complement can promote a diversity of human inflammatory diseases which are treated by complement inhibitors. Here, we generated a novel blocking monoclonal antibody (mAb) against properdin and devised a new diagnostic assay for this important complement regulator. Mouse mAb 1340 specifically detected native properdin from human samples with high avidity. MAb 1340 inhibited specifically the alternative complement mediated cell lysis within a concentration range of 1-10 µg/mL. Thus, in vitro anti-properdin mAb 1340 was up to fifteen times more efficient in blocking the complement system as compared to anti-C5 or anti-Ba antibodies. Computer-assisted modelling suggested a three-dimensional binding epitope in a properdin-C3(H2O)-clusterin complex to be responsible for the inhibition. Recovery of properdin in a newly established sandwich ELISA using mAb 1340 was determined at 80-125% for blood sample dilutions above 1∶50. Reproducibility assays showed a variation below 25% at dilutions less than 1∶1,000. Systemic properdin concentrations of healthy controls and patients with age-related macular degeneration or rheumatic diseases were all in the range of 13-30 µg/mL and did not reveal significant differences. These initial results encourage further investigation into the functional role of properdin in the development, progression and treatment of diseases related to the alternative complement pathway. Thus, mAb 1340 represents a potent properdin inhibitor suitable for further research to understand the exact mechanisms how properdin activates the complement C3-convertase and to determine quantitative levels of properdin in biological samples.

Indexed as

AnimalsAntibodies, MonoclonalComplement Pathway, AlternativeComputer SimulationEnzyme-Linked Immunosorbent AssayHumansImmunity, InnateMiceModels, ImmunologicalModels, MolecularProperdinReproducibility of ResultsAntibodies, MonoclonalProperdin

Identifiers

PMID24797388
PMCPMC4010523
OpenAlexW2068258578

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.