Evidence map›Paper›PMID 12813023›Full record

ArticleThe Journal of clinical investigation2003

Complement receptor 2-mediated targeting of complement inhibitors to sites of complement activation.

Hongbin Song, Chun He, Christian Knaak, Joel M Guthridge, V Michael Holers, Stephen Tomlinson

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
1.8field-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

62 citing papers in PubMed, 113 citations in OpenAlex.

  1. Article
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  9. Increasing the efficacy and safety of a human complement inhibitor for treating post-transplant cardiac ischemia reperfusion injury by targeting to a graft-specific neoepitope.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2021
    Article
  10. Article
  11. Article
  12. Review
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  14. Article
  15. Article
  16. Review
  17. Review
  18. Complement C3-Targeted Gene Therapy Restricts Onset and Progression of Neurodegeneration in Chronic Mouse Glaucoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
    Article
  19. Tissue-targeted complement therapeutics.Molecular immunology · 2018
    Review
  20. Article

2 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

6 authors at 2 institutions in 1 country.

Hongbin SongDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Chun He
Christian Knaak
Joel M Guthridge
V Michael Holers
Stephen Tomlinson
Medical University of South Carolina · USUniversity of Colorado Health · US

Funding

C3D/EBV RECEPTOR LIGAND BINDING SITESR01CA053615 · NCI · WASHINGTON UNIVERSITY · PI HOLERS, VERNON MICHAEL · 1991 to 2006
$1.7M
TARGETED COMPLEMENT INHIBITORSR01AI034451 · NIAID · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TOMLINSON, STEPHEN · 2000 to 2003
$1.0M
MECHANISM OF ACTION OF CD59R29AI034451 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TOMLINSON, STEPHEN · 1994 to 1998
–
NCI NIH HHS CA53615NCI NIH HHS R01 CA053615NIAID NIH HHS AI 34451NIAID NIH HHS R01 AI034451NIAID NIH HHS R29 AI034451
6 · The paper itself

Abstract

In a strategy to specifically target complement inhibitors to sites of complement activation and disease, recombinant fusion proteins consisting of a complement inhibitor linked to a C3 binding region of complement receptor (CR) 2 were prepared and characterized. Natural ligands for CR2 are C3 breakdown products deposited at sites of complement activation. Fusion proteins were prepared consisting of a human CR2 fragment linked to either the N terminus or C terminus of soluble forms of the membrane complement inhibitors decay accelerating factor (DAF) or CD59. The targeted complement inhibitors bound to C3-opsonized cells, and all were significantly more effective (up to 20-fold) than corresponding untargeted inhibitors at protecting target cells from complement. CR2 fusion proteins also inhibited CR3-dependent adhesion of U937 cells to C3 opsonized erythrocytes, indicating a second potential anti-inflammatory mechanism of CR2 fusion proteins, since CR3 is involved in endothelial adhesion and diapedesis of leukocytes at inflammatory sites. Finally, the in vivo validity of the targeting strategy was confirmed by the demonstration that CR2-DAF, but not soluble DAF, targets to the kidney in mouse models of lupus nephritis that are associated with renal complement deposition.

Indexed as

Complement ActivationAnimalsCD55 AntigensCD59 AntigensCell AdhesionCHO CellsComplement C3Complement Inactivator ProteinsCricetinaeErythrocytesFemaleHumansIn Vitro TechniquesKidneyLigandsLupus NephritisCD55 AntigensCD59 AntigensComplement C3Complement Inactivator ProteinsLigandsReceptors, Complement 3dRecombinant Fusion Proteins

Identifiers

PMID12813023
PMCPMC161422
OpenAlexW2150659072

What OpenQuestion holds

Textmetadata
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.