Evidence map›Paper›PMID 21918195›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Deletion of Syk in neutrophils prevents immune complex arthritis.

Emily R Elliott, Jessica A Van Ziffle, Patrizia Scapini, Brandon M Sullivan, Richard M Locksley, Clifford A Lowell

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

55 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Review
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  8. Article
  9. Article
  10. Review
  11. Neutrophil extracellular traps impair regeneration.Journal of cellular and molecular medicine · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Neutrophils as emerging therapeutic targets.Nature reviews. Drug discovery · 2020
    Review
  16. Review
  17. Review
  18. Review
  19. Mouse Models and Tools for theFrontiers in immunology · 2019
    Review
  20. Review
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 3 institutions in 1 country.

Emily R ElliottBiomedical Sciences Program, University of California, San Francisco, San Francisco, CA 94143, USA.
Jessica A Van Ziffle
Patrizia Scapini
Brandon M Sullivan
Richard M Locksley
Clifford A Lowell
University of California, San Francisco · USUniversity of San Francisco · USHoward Hughes Medical Institute · US

Funding

The contribution of innate immune cells to autoimmunityP01AI078869 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2008 to 2012
$8.9M
Mechanisms of Neutrophil ActivationR01AI065495 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2005 to 2017
$3.7M
Signaling by Cytoplasmic Tyrosine Kinases in LeukocytesR01AI068150 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2006 to 2016
$3.4M
Howard Hughes Medical InstituteNIAID NIH HHS AI65495NIAID NIH HHS AI68150NIAID NIH HHS P01 AI078869NIAID NIH HHS R01 AI065495NIAID NIH HHS R01 AI068150
6 · The paper itself

Abstract

The K/BxN serum transfer model of arthritis is critically dependent on FcγR signaling events mediated by spleen tyrosine kinase (Syk). However, the specific cell types in which this signaling is required are not known. We report that deletion of Syk in neutrophils, achieved using syk(f/f) MRP8-cre(+) mice, blocks disease development in serum transfer arthritis. The syk(f/f) MRP8-cre(+) mice display absent joint disease and reduced deposition of pathogenic anti-glucose-6-phosphate isomerase Abs in the joint (with a reciprocal accumulation of these Abs in the peripheral circulation). Additionally, syk(f/f) MRP8-cre(+) mice manifest poor edema formation within 3 h after formation of cutaneous immune complexes (Arthus reaction). Together, this suggests that neutrophil-dependent recognition of immune complexes contributes significantly to changes in vascular permeability during the early phases of immune complex disease. Using mixed chimeric mice, containing both wild-type and syk(f/f) MRP8-cre(+) neutrophils, we find no impairment in recruitment of Syk-deficient neutrophils to the inflamed joint, but they fail to become primed, demonstrating lower cytokine production after removal from the joint. They also display an increased apoptotic rate compared with wild-type cells in the same joint. Mast cell-deficient c-kit(sh/sh) mice developed robust arthritis after serum transfer whereas c-kit(W/Wv) mice did not, suggesting that previous conclusions concerning the central role of mast cells in this model may need to be revised. Basophil-deficient mice also responded normally to K/BxN serum transfer. These results demonstrate that Syk-dependent signaling in neutrophils alone is critically required for arthritis development in the serum transfer model.

Indexed as

AnimalsArthritis, ExperimentalArthus ReactionCell SeparationEnzyme-Linked Immunosorbent AssayFlow CytometryFluorescent Antibody TechniqueIntracellular Signaling Peptides and ProteinsMast CellsMiceMice, Inbred C57BLNeutrophilsProtein-Tyrosine KinasesSignal TransductionSyk KinaseIntracellular Signaling Peptides and ProteinsProtein-Tyrosine KinasesSyk KinaseSyk protein, mouse

Identifiers

PMID21918195
PMCPMC3186826
OpenAlexW2149476900

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.