Evidence map›Paper›PMID 22392608›Full record

ArticleArthritis and rheumatism2012

A functional variant in FCRL3 is associated with higher Fc receptor-like 3 expression on T cell subsets and rheumatoid arthritis disease activity.

Urmila D Bajpai, Louise A Swainson, Jeff E Mold, Jonathan D Graf, John B Imboden, Joseph M McCune

Open access · greenAbstract readComparative Study
In one paragraph

Article in Arthritis and rheumatism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. Association ofFrontiers in bioinformatics · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Impacts of rs7528684 (-169T/C) onFrontiers in genetics · 2025
    Article
  9. Review
  10. Advances in mesenchymal stem cells therapy for tendinopathies.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2024
    Review
  11. Article
  12. Sjögren's Syndrome Minor Salivary Gland CD4Journal of clinical medicine · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Human FcR polymorphism and disease.Current topics in microbiology and immunology · 2014
    Review
  20. Emerging roles for the FCRL family members in lymphocyte biology and disease.Current topics in microbiology and immunology · 2014
    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 1 institution in 1 country.

Urmila D BajpaiUniversity of California, San Francisco, CA 94110, USA.
Louise A Swainson
Jeff E Mold
Jonathan D Graf
John B Imboden
Joseph M McCune
University of California, San Francisco · US

Funding

UCSF CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTEUL1RR024131 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JOHNSTON, S. CLAIBORNE · 2006 to 2011
$111.2M
NIH Director's Pioneer Award (RMI)DP1OD000329 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MCCUNE, JOSEPH M · 2004 to 2008
$4.2M
NCRR NIH HHS UL1 RR024131NCRR NIH HHS UL1-RR-024131NIH HHS DP1 OD000329NIH HHS DPI-OD-00329
6 · The paper itself

Abstract

objectiveCD4+FoxP3+ Treg cells suppress effector T cells and prevent autoimmune disease. Treg cell function is deficient in active rheumatoid arthritis (RA), a loss which may play a role in the pathogenesis of this disease. We previously showed that a single-nucleotide polymorphism in the FCRL3 gene led to higher expression of Fc receptor-like 3 (FcRL3) on Treg cells and that FcRL3+ Treg cells are functionally deficient in comparison to FcRL3- Treg cells. This study was undertaken to investigate the potential role of FcRL3 in RA.

methodsA cross-sectional study was performed to evaluate the FCRL3 -169 genotype and FcRL3 expression on T cell subsets, including Treg cells, in peripheral blood samples from 51 patients with RA enrolled in the University of California, San Francisco (UCSF) RA Cohort. Clinical data were obtained from the UCSF RA Cohort database.

resultsPatients with the FCRL3 -169C allele (genotype C/C or C/T) expressed higher levels of FcRL3 on Treg cells, and on CD8+ and γ/δ T cells, in comparison to RA patients with the T/T genotype. Higher FcRL3 expression on these T cell subpopulations correlated with RA disease activity in patients harboring the FCRL3 -169C allele. Furthermore, FcRL3 expression on Treg cells was higher in patients with erosive RA, and the FCRL3 -169C allele was overrepresented in patients with erosive RA.

conclusionOur findings indicate that FcRL3 expression, which is strongly associated with the presence of the FCRL3 -169C allele, may serve as a biomarker for RA disease activity.

Indexed as

Severity of Illness IndexAdultAllelesArthritis, RheumatoidBiomarkersB-LymphocytesCD8 AntigensCell CountCross-Sectional StudiesFemaleGenotypeHumansMaleMiddle AgedPolymorphism, Single NucleotideReceptors, Antigen, T-Cell, gamma-deltaBiomarkersCD8 AntigensFCRL3 protein, humanReceptors, Antigen, T-Cell, gamma-deltaReceptors, Immunologic

Identifiers

PMID22392608
PMCPMC3374037
OpenAlexW2007362634

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.