Evidence map›Paper›PMID 22393153›Full record

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

Inhibition of epidermal growth factor receptor tyrosine kinase ameliorates collagen-induced arthritis.

Christina D Swanson, Elliot H Akama-Garren, Emily A Stein, Jacob D Petralia, Pedro J Ruiz, Abdolhossein Edalati, Tamsin M Lindstrom, William H Robinson

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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The 'autoimmunome' of centenarians.Journal of translational autoimmunity · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
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  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Metabolites · 2020
    Article
  19. Observational
  20. Amphiregulin Aggravates GlomerulonephritisJournal of the American Society of Nephrology : JASN · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Christina D SwansonDivision of Immunology and Rheumatology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. christina.d.swanson@gmail.com
Elliot H Akama-Garren
Emily A Stein
Jacob D Petralia
Pedro J Ruiz
Abdolhossein Edalati
Tamsin M Lindstrom
William H Robinson
VA Palo Alto Health Care System · USStanford University · US

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Tyrosine Kinase Pathways in Rheumatoid ArthritisR01AR054822 · NIAMS · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI ROBINSON, WILLIAM H · 2007 to 2011
$1.5M
NHLBI NIH HHS N01-HV-00242NIAID NIH HHS 5 T32 AI07290NIAID NIH HHS T32 AI007290NIAMS NIH HHS R01 AR-054822NIAMS NIH HHS R01 AR054822
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune synovitis characterized by the formation of pannus and the destruction of cartilage and bone in the synovial joints. Although immune cells, which infiltrate the pannus and promote inflammation, play a prominent role in the pathogenesis of RA, other cell types also contribute. Proliferation of synovial fibroblasts, for example, underlies the formation of the pannus, while proliferation of endothelial cells results in neovascularization, which supports the growth of the pannus by supplying it with nutrients and oxygen. The synovial fibroblasts also promote inflammation in the synovium by producing cytokines and chemokines. Finally, osteoclasts cause the destruction of bone. In this study, we show that erlotinib, an inhibitor of the tyrosine kinase epidermal growth factor receptor (EGFR), reduces the severity of established collagen-induced arthritis, a mouse model of RA, and that it does so by targeting synovial fibroblasts, endothelial cells, and osteoclasts. Erlotinib-induced attenuation of autoimmune arthritis was associated with a reduction in number of osteoclasts and blood vessels, and erlotinib inhibited the formation of murine osteoclasts and the proliferation of human endothelial cells in vitro. Erlotinib also inhibited the proliferation and cytokine production of human synovial fibroblasts in vitro. Moreover, EGFR was highly expressed and activated in the synovium of mice with collagen-induced arthritis and patients with RA. Taken together, these findings suggest that EGFR plays a central role in the pathogenesis of RA and that EGFR inhibition may provide benefits in the treatment of RA.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidBecaplerminCell DivisionCyclooxygenase 2CytokinesDrug Evaluation, PreclinicalEndothelial CellsErbB ReceptorsErlotinib HydrochlorideFibroblastsGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsMale4-((3-bromophenyl)amino)-6,7-dimethoxyquinazolineBecaplerminCyclooxygenase 2CytokinesEGFR protein, humanEGFR protein, mouseErbB ReceptorsErlotinib HydrochlorideProtein Kinase InhibitorsProto-Oncogene Proteins c-sisPtgs2 protein, mouseQuinazolines

Identifiers

PMID22393153
PMCPMC3311775
OpenAlexW2132650643

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.