Evidence map›Paper›PMID 17916747›Full record

ArticleBlood2008

Activator-specific requirement of properdin in the initiation and amplification of the alternative pathway complement.

Yuko Kimura, Takashi Miwa, Lin Zhou, Wen-Chao Song

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

65 citing papers in PubMed, 118 citations in OpenAlex.

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  18. Review
  19. Review
  20. Human Properdin Modulates Macrophage:Frontiers in immunology · 2018
    Article

5 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

4 authors at 2 institutions in 1 country.

Yuko KimuraInstitute for Translational Medicine and Therapeutics, Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia 19104, USA.
Takashi Miwa
Lin Zhou
Wen-Chao Song
Translational Therapeutics (United States) · USUniversity of Pennsylvania · US

Funding

BIOLOGY OF DECAY ACCELERATING FACTORR01AI044970 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SONG, WENCHAO · 2000 to 2014
$4.9M
Complement Regulatory Proteins and Autoimmune DiseaseR01AI049344 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SONG, WENCHAO · 2002 to 2011
$3.3M
Rapid Acting Vaccine for Pandemic InfluenzaUC1AI062388 · NIAID · CORIXA CORPORATION · PI CIEPLAK, WITOLD · 2005 to 2005
$2.7M
Complement Regulatory Proteins and Autoimmune DiseaseR21AI049344 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SONG, WENCHAO · 2001 to 2001
$302k
NIAID NIH HHS AI-44970NIAID NIH HHS AI-49344NIAID NIH HHS AI-62388NIAID NIH HHS R01 AI044970NIAID NIH HHS R01 AI049344NIAID NIH HHS R21 AI049344NIAID NIH HHS UC1 AI062388
6 · The paper itself

Abstract

Properdin is a positive regulator of alternative pathway (AP) complement. The current understanding of properdin function is that it facilitates AP complement activation by stabilizing the C3 convertase C3bBb. Properdin-deficient patients are susceptible to lethal meningococcal infection, but the mechanism of this selective predisposition is not fully understood. By gene targeting in the mouse, we show here that properdin is essential for AP complement activation induced by bacterial lipopolysacharride (LPS) and lipooligosacharride (LOS) and other, but not all, AP complement activators. LPS- and LOS-induced AP complement activation was abolished in properdin-/- mouse serum, and properdin-/- mice were unable to clear Crry-deficient erythrocytes, which are known to be susceptible to AP complement-mediated extravascular hemolysis. In contrast, zymosan- and cobra venom factor-induced AP complement activation, and classical pathway-triggered AP complement amplification were only partially or minimally affected in properdin-/- mice. We further show that the ability of human properdin to restore LPS-dependent AP complement activity in properdin-/- mouse serum correlated with the human properdin-binding affinity of the LPS. These results reveal a novel role of properdin in AP complement initiation and have implications for understanding the selective predisposition of properdin-deficient patients to meningococcal infection.

Indexed as

Complement Pathway, AlternativeAnimalsComplement C3 Convertase, Alternative PathwayGene TargetingGenetic Predisposition to DiseaseHumansLipopolysaccharidesMeningococcal InfectionsMiceMice, KnockoutProperdinReceptors, ComplementReceptors, Complement 3bComplement C3 Convertase, Alternative PathwayCR1L protein, humanCr1l protein, mouseLipopolysaccharidesProperdinReceptors, ComplementReceptors, Complement 3b

Identifiers

PMID17916747
PMCPMC2200840
OpenAlexW1986714262

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.