Evidence map›Paper›PMID 20580090›Full record

ReviewMolecular immunology2010

Complement control protein factor H: the good, the bad, and the inadequate.

Viviana P Ferreira, Michael K Pangburn, Claudio Cortés

Open access · greenAbstract readReview
In one paragraph

Review in Molecular immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

224 citing papers in PubMed, 1 synthesis or guideline pooled it, 415 citations in OpenAlex.

  1. Pooled it
  2. Complement-Regulatory Proteins CFHR1 and CFHR3 and Patient Response to Anti-CD20 Monoclonal Antibody Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
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  7. Review
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  12. Review
  13. Frontiers in immunology · 2026
    Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
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  20. Article

164 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

3 authors at 3 institutions in 1 country.

Viviana P FerreiraDepartment of Medical Microbiology and Immunology, College of Medicine, University of Toledo, Toledo, OH 43614, United States. viviana.ferreira@utoledo.edu
Michael K Pangburn
Claudio Cortés
The University of Texas Health Science Center at Tyler · USUniversity of Toledo · USUniversity of Toledo Medical Center · US

Funding

REGULATION OF COMPLEMENT BY MEMBRANE PROTEINSR01DK035081 · NIDDK · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI PANGBURN, MICHAEL K. · 1986 to 2011
$2.5M
The role of complement proteins in cardiovascular diseaseP30HL101317 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI TAKASHIMA, AKIRA · 2009 to 2010
$1.2M
ACTIVATION OF THE ALTERNATIVE PATHWAY OF COMPLEMENTR37DK035081 · NIDDK · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI PANGBURN, MICHAEL K. · 1993 to 2000
$206k
NHLBI NIH HHS 1P30HL101317-01NHLBI NIH HHS P30 HL101317NIDDK NIH HHS DK-35081NIDDK NIH HHS R01 DK035081NIDDK NIH HHS R37 DK035081
6 · The paper itself

Abstract

The complement system is an essential component of the innate immune system that participates in elimination of pathogens and altered host cells and comprises an essential link between the innate and adaptive immune system. Soluble and membrane-bound complement regulators protect cells and tissues from unintended complement-mediated injury. Complement factor H is a soluble complement regulator essential for controlling the alternative pathway in blood and on cell surfaces. Normal recognition of self-cell markers (i.e. polyanions) and C3b/C3d fragments is necessary for factor H function. Inadequate recognition of host cell surfaces by factor H due to mutations and polymorphisms have been associated with complement-mediated tissue damage and disease. On the other hand, unwanted recognition of pathogens and altered self-cells (i.e. cancer) by factor H is used as an immune evasion strategy. This review will focus on the current knowledge related to these versatile recognition properties of factor H.

Indexed as

AnimalsComplement C3bComplement C3dComplement Factor HComplement Pathway, AlternativeHumansImmune EvasionModels, ImmunologicalProtein BindingComplement C3bComplement C3dComplement Factor H

Identifiers

PMID20580090
PMCPMC2921957
OpenAlexW2133876809

What OpenQuestion holds

Textmetadata
LicenceTDM
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.