Evidence map›Paper›PMID 18684964›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Membrane protein Crry maintains homeostasis of the complement system.

Xiaobo Wu, Dirk Spitzer, Dailing Mao, Stanford L Peng, Hector Molina, John P Atkinson

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Timing and mechanism of conceptus demise in a complement regulatory membrane protein deficient mouse.American journal of reproductive immunology (New York, N.Y. : 1989) · 2018
    Article
  5. Complement activation, a threat to pregnancy.Seminars in immunopathology · 2018
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. C3-dependent mechanism of microglial priming relevant to multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  13. Structures of the rat complement regulator CrrY.Acta crystallographica. Section F, Structural biology and crystallization communications · 2011
    Article
  14. Properdin homeostasis requires turnover of the alternative complement pathway.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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 1 institution in 1 country.

Xiaobo WuDepartment of Medicine, Division of Rheumatology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Dirk Spitzer
Dailing Mao
Stanford L Peng
Hector Molina
John P Atkinson
Washington University in St. Louis · US

Funding

Complement Receptor One (CRI): Structure/FunctionR01AI041592 · NIAID · WASHINGTON UNIVERSITY · PI ATKINSON, JOHN · 1997 to 2013
$3.9M
MCP--STRUCTURE, MICROBIAL INTERACTIONS AND FUNCTIONR01AI037618 · NIAID · WASHINGTON UNIVERSITY · PI ATKINSON, JOHN · 1995 to 2010
$3.3M
NIAID NIH HHS R01 AI037618NIAID NIH HHS R01-AI037618NIAID NIH HHS R01 AI041592NIAID NIH HHS R01-AI041592
6 · The paper itself

Abstract

Complement activation is tightly regulated to avoid excessive inflammatory and immune responses. Crry(-/-) is an embryonic lethal phenotype secondary to the maternal complement alternative pathway (AP) attacking a placenta deficient in this inhibitor. In this study, we demonstrate that Crry(-/-) mice could be rescued on a partial as well as on a complete factor B (fB)- or C3-deficient maternal background. The C3 and fB protein concentrations in Crry(-/-)C3(+/-) and Crry(-/-)fB(+/-) mice were substantially reduced for gene dosage secondary to enhanced AP turnover. Based on these observations, a breeding strategy featuring reduced maternal AP-activating capacity rescued the lethal phenotype. It led to a novel, stable line of Crry SKO mice carrying normal alleles for C3 and fB. Crry SKO mice also had accelerated C3 and fB turnover and therefore reduced AP- activating potential. These instructive results represent an example of a membrane regulatory protein being responsible for homeostasis of the complement system. They imply that there is constant turnover on cells of the AP pathway which functions as an immune surveillance system for pathogens and altered self.

Indexed as

AnimalsCell LineComplement C3Complement Factor BComplement Pathway, AlternativeEmbryo LossFemaleGenotypeHomeostasisHumansMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutReceptors, ComplementComplement C3Complement Factor BCr1l protein, mouseMembrane ProteinsReceptors, ComplementReceptors, Complement 3b

Identifiers

PMID18684964
PMCPMC2580744
OpenAlexW2131613225

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.