Evidence map›Paper›PMID 22205026›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Role of C3a receptors, C5a receptors, and complement protein C6 deficiency in collagen antibody-induced arthritis in mice.

Nirmal K Banda, Stephanie Hyatt, Alexandra H Antonioli, Jason T White, Magdalena Glogowska, Kazue Takahashi, Tod J Merkel, Gregory L Stahl, Stacey Mueller-Ortiz, Rick Wetsel and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
4.1field-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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

14 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

12 authors at 6 institutions in 1 country.

Nirmal K BandaDivision of Rheumatology, Department of Medicine and Immunology, University of Colorado School of Medicine, Aurora, CO 80045, USA.
Stephanie Hyatt
Alexandra H Antonioli
Jason T White
Magdalena Glogowska
Kazue Takahashi
Tod J Merkel
Gregory L Stahl
Stacey Mueller-Ortiz
Rick Wetsel
William P Arend
V Michael Holers
University of Colorado Denver · USBrigham and Women's Hospital · USCenter for Biologics Evaluation and Research · USMassachusetts General Hospital · USTexas Research Institute · USUniversity of Houston · US

Funding

Medical Scientist Training ProgramT32GM008497 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI WILSON, CARA C. · 1993 to 2022
$15.2M
Complement in the Pathogenesis of Autoimmune ArthritisR01AR051749 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI Vernon Michael Holers · 2004 to 2026
$6.7M
Research Training in Rheumatology INCLUDE Down Syndrome SupplementT32AR007534 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI Kristine A. Kuhn · 1986 to 2026
$6.1M
Complement in the Pathogenesis of Autoimmune ArthritisR56AR051749 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI HOLERS, VERNON MICHAEL · 2020 to 2020
$342k
NIAMS NIH HHS AR051749NIAMS NIH HHS R01 AR051749NIAMS NIH HHS R56 AR051749NIAMS NIH HHS T32 AR007534NIGMS NIH HHS T32 GM008497
6 · The paper itself

Abstract

The complement system, especially the alternative pathway, plays essential roles in the induction of injury in collagen Ab-induced arthritis (CAIA) in mice. The goal of the current study was to directly compare the roles of receptors for C3a and C5a, as well as the membrane attack complex, as effector mechanisms in the pathogenesis of CAIA. Clinical disease activity in C3aR(-/-), C5aR(-/-), and C6-deficient (C6-def) mice was decreased by 52, 94, and 65%, respectively, as compared with wild-type mice. Decreases in histopathologic injury as well as in IgG and C3 deposition paralleled the clinical disease activity. A decrease in the percentage of synovial neutrophils was observed in C3aR(-/-), C5aR(-/-), and C6-def mice, and a decrease in macrophages was observed in C3aR(-/-) and C5aR(-/-), but not in C6-def, mice. Synovial mRNA obtained by laser capture microdissection exhibited a decrease in TNF-α in C5aR(-/-) mice and in IL-1β in both C5aR(-/-) and C6-def mice, whereas C3aR(-/-) mice demonstrated no change in either cytokine. Our findings show that absent C3aR-, C5aR-, or membrane attack complex-initiated effector mechanisms each decrease susceptibility to CAIA, with clinical effects most pronounced in C5aR-deficient mice. Although the absence of C3aR, C5aR, or C6 led to differential deficiencies in effector mechanisms, decreased proximal joint IgG and C3 deposition was common to all three genotypes in comparison with wild-type mice. These data suggest the existence of positive-feedback amplification pathways downstream of all three effectors that promote additional IgG deposition and C3 activation in the joint.

Indexed as

AnimalsArthritis, ExperimentalComplement ActivationComplement C3aComplement C6CytokinesDisease SusceptibilityImmunoglobulin GMacrophagesMiceMice, KnockoutNeutrophilsReceptor, Anaphylatoxin C5aReceptors, ComplementSynovial FluidComplement C3acomplement C3a receptorComplement C6CytokinesImmunoglobulin GReceptor, Anaphylatoxin C5aReceptors, Complement

Identifiers

PMID22205026
PMCPMC3262949
OpenAlexW2155546923

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.