Evidence map›Paper›PMID 27546448›Full record

ArticleClinical immunology (Orlando, Fla.)2016

Compstatin Cp40 blocks hematin-mediated deposition of C3b fragments on erythrocytes: Implications for treatment of malarial anemia.

Margaret A Lindorfer, Erika M Cook, Edimara S Reis, Daniel Ricklin, Antonio M Risitano, John D Lambris, Ronald P Taylor

Open access · greenAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury.International journal of biological sciences · 2021
    Review
  4. COVID 19: a clue from innate immunity.Immunologic research · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. P-selectin drives complement attack on endothelium during intravascular hemolysis in TLR-4/heme-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

7 authors at 2 institutions in 1 country.

Margaret A LindorferDepartment of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, United States.
Erika M CookDepartment of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, United States.
Edimara S ReisDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, United States.
Daniel RicklinDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, United States.
Antonio M RisitanoHematology, Department of Clinical Medicine and Surgery, Federico II University of Naples, Italy.
John D LambrisDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, United States.
Ronald P TaylorDepartment of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, United States. Electronic address: rpt@virginia.edu.
University of Pennsylvania · USUniversity of Virginia · US

Funding

Role of complement in kidney disorders: from hemodialysis to transportationP01AI068730 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2007 to 2018
$16.0M
STRUCTURE-FUNCTION ANALYSIS OF DIFFERENT C3 SPECIESR01AI030040 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 1993 to 2016
$4.1M
VIRAL RESPIRATORY PATHOGENS RESEARCH UNIT /VRPRU/-266030040-266030040N01AI030040 · NIAID · UNIVERSITY OF IOWA · PI APICELLA, MICHAEL A. · 2003 to 2006
–
NIAID NIH HHS N01 AI030040NIAID NIH HHS P01 AI068730NIAID NIH HHS R01 AI030040
6 · The paper itself

Abstract

During malarial anemia, 20 uninfected red blood cells (RBCs) are destroyed for every RBC infected by Plasmodium falciparum (Pf). Increasing evidence indicates an important role for complement in destruction of uninfected RBCs. Products of RBC lysis induced by Pf, including the digestive vacuole and hematin, activate complement and promote C3 fragment deposition on uninfected RBCs. C3-opsonized cells are then subject to extravascular destruction mediated by fixed tissue macrophages which express receptors for C3 fragments. The Compstatin family of cyclic peptides blocks complement activation at the C3 cleavage step, and is under investigation for treatment of complement-mediated diseases. We demonstrate, that under a variety of stringent conditions, second-generation Compstatin analogue Cp40 completely blocks hematin-mediated deposition of C3 fragments on naïve RBCs. Our findings indicate that prophylactic provision of Compstatin for malaria-infected individuals at increased risk for anemia may provide a safe and inexpensive treatment to prevent or substantially reduce malarial anemia.

Indexed as

AnemiaComplement C3bErythrocytesHeminHumansMalaria, FalciparumPeptides, CyclicPlasmodium falciparumComplement C3bcompstatinHeminPeptides, CyclicComplementCompstatinHematinMalarial anemia

Identifiers

PMID27546448
PMCPMC5330307
OpenAlexW2508009130

What OpenQuestion holds

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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.