Evidence map›Paper›PMID 24462362›Full record

ArticleBiomaterials2014

Mediation of a non-proteolytic activation of complement component C3 by phospholipid vesicles.

Yvonne Klapper, Osama A Hamad, Yuji Teramura, Gero Leneweit, G Ulrich Nienhaus, Daniel Ricklin, John D Lambris, Kristina N Ekdahl, Bo Nilsson

Open access · greenAbstract read
In one paragraph

Article in Biomaterials, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 49 citations in OpenAlex.

  1. Liposomes in tumor treatment: a double-edged sword.Science China. Life sciences · 2026
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  7. Complement opsonization of nanoparticles: Differences between humans and preclinical species.Journal of controlled release : official journal of the Controlled Release Society · 2021
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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

9 authors at 4 institutions in 4 countries.

Yvonne KlapperInstitute of Applied Physics and Center for Functional Nanostructures (CFN), Karlsruhe Institute of Technology (KIT), Wolfgang-Gaede-Str. 1, 76131 Karlsruhe, Germany; Carl Gustav Carus-Institute, Association for the Promotion of Cancer Therapy, Am Eichhof 30, 75223 Niefern-Öschelbronn, Germany; Department of Immunology, Genetics and Pathology, Rudbeck Laboratory C5:3, Uppsala University, 75185 Uppsala, Sweden.
Osama A HamadDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory C5:3, Uppsala University, 75185 Uppsala, Sweden.
Yuji TeramuraDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory C5:3, Uppsala University, 75185 Uppsala, Sweden; Department of Bioengineering, The University of Tokyo, 7-3-1 Hongo, Bunkyo-Ku, Tokyo 113-8656, Japan.
Gero LeneweitCarl Gustav Carus-Institute, Association for the Promotion of Cancer Therapy, Am Eichhof 30, 75223 Niefern-Öschelbronn, Germany.
G Ulrich NienhausInstitute of Applied Physics and Center for Functional Nanostructures (CFN), Karlsruhe Institute of Technology (KIT), Wolfgang-Gaede-Str. 1, 76131 Karlsruhe, Germany; Department of Physics, University of Illinois at Urbana-Champaign, 1110 W. Green Street, Urbana, IL 61801, USA; Institute of Toxicology and Genetics, Karlsruhe Institute of Technology (KIT), Hermann-von-Helmholtz-Platz 1, 76344 Eggenstein-Leopoldshafen, Germany.
Daniel RicklinDepartment of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
John D LambrisDepartment of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Kristina N EkdahlDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory C5:3, Uppsala University, 75185 Uppsala, Sweden; Linnæus Center of Biomaterials Chemistry, Linnæus University, 39182 Kalmar, Sweden.
Bo NilssonDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory C5:3, Uppsala University, 75185 Uppsala, Sweden. Electronic address: bo.nilsson@igp.uu.se.
Uppsala University · SEKarlsruhe Institute of Technology · DEUniversity of Pennsylvania · USCarl Gustav Carus-Institut · DE

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
HIV VACCINE DESIGN AND DEVELOPMENT TEAMS (HVDDT)-266030030N01AI030030 · NIAID · PROGENICS PHARMACEUTICALS, INC · PI MADDON, PAUL J · 2003 to 2003
–
NIAID NIH HHS AI030030NIAID NIH HHS AI068730NIAID NIH HHS N01 AI030030NIAID NIH HHS P01 AI068730NIAID NIH HHS R01 AI030040
6 · The paper itself

Abstract

Liposomes are becoming increasingly important as drug delivery systems, to target a drug to specific cells and tissues and thereby protecting the recipient from toxic effects of the contained drug. Liposome preparations have been described to activate complement. In this study, we have investigated complement activation triggered by neutral dimyristoyl-phosphocholine (DMPC) liposomes in human plasma and whole-blood systems. Incubation in plasma led to the generation of complement activation products (C3a and sC5b-9). Unexpectedly, investigations of surface-bound C3 revealed contact activated, conformationally changed C3 molecules on the liposomes. These changes were characterized by Western blotting with C3 monoclonal antibodies, and by incubating liposomes with purified native C3 and factors I and H. Quartz crystal microbalance analysis confirmed binding of C3 to planar DMPC surfaces. In addition, we demonstrated that DMPC liposomes bound to or were phagocytized by granulocytes in a complement-dependent manner, as evidenced by the use of complement inhibitors. In summary, we have shown that C3 is activated both by convertase-dependent cleavage, preferentially in the fluid phase, by mechanisms which are not well elucidated, and also by contact activation into C3(H2O) on the DMPC surface. In particular, this contact activation has implications for the therapeutic regulation of complement activation during liposome treatment.

Indexed as

AdsorptionComplement ActivationComplement C3Computer SystemsDimyristoylphosphatidylcholineElectrophoresis, Polyacrylamide GelFlow CytometryHumansLiposomesModels, BiologicalPhagocytosisPhospholipidsProtein BindingProteolysisQuartz Crystal Microbalance TechniquesComplement C3DimyristoylphosphatidylcholineLiposomesPhospholipidsComplementContact activationImmune responseLiposome

Identifiers

PMID24462362
PMCPMC4104820
OpenAlexW2167933060

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.