Evidence map›Paper›PMID 20190142›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Expression of the autoimmune susceptibility gene FcRL3 on human regulatory T cells is associated with dysfunction and high levels of programmed cell death-1.

Louise A Swainson, Jeff E Mold, Urmila D Bajpai, Joseph M McCune

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
3.3field-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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Impacts of rs7528684 (-169T/C) onFrontiers in genetics · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. CD4 T-Cell Exhaustion: Does It Exist and What Are Its Roles in Cancer?Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. The Ligands for Human IgG and Their Effector Functions.Antibodies (Basel, Switzerland) · 2019
    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

4 authors at 1 institution in 1 country.

Louise A SwainsonDivision of Experimental Medicine, Department of Medicine, University of California at San Francisco, San Francisco, CA 94110, USA.
Jeff E Mold
Urmila D Bajpai
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
Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STEVEN Grant DEEKS · 1988 to 2026
$93.6M
HIV EFFECTS ON THE CENTRAL HEMATOLYMPHOID SYSTEMR37AI040312 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MCCUNE, JOSEPH M · 2000 to 2010
$5.0M
UCSF-GIVI CENTER FOR AIDS RESEARCHP30MH059037 · NIMH · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI FEINBERG, MARK A · 1998 to 2001
$4.9M
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 RR024131NIAID NIH HHS P30 AI027763NIAID NIH HHS R37 AI040312NIAID NIH HHS R37 AI40312NIH HHS DP1 OD000329NIH HHS DPI OD00329NIMH NIH HHS P30 MH059037NIMH NIH HHS P30 MH59037
6 · The paper itself

Abstract

CD4(+)FoxP3(+) regulatory T cells (T(reg)) play a critical role in maintaining self-tolerance and inhibiting autoimmune disease. Despite being a major focus of modern immunological investigation, many aspects of T(reg) biology remain unknown. In a screen for novel candidate genes involved in human T(reg) function, we detected the expression of an autoimmune susceptibility gene, FcRL3, in T(reg) but not in conventional CD4(+) T cells. FcRL3 is an orphan receptor of unknown function with structural homology to classical Fc receptors. Numerous genetic studies have demonstrated a link between a single nucleotide polymorphism in the FCRL3 promoter and both overexpression of FcRL3 and autoimmune diseases such as rheumatoid arthritis. Given the critical role of T(reg) in suppressing autoimmunity, we sought to ascertain how expression of FcRL3 relates to the phenotype, differentiation, and function of T(reg). We show in this study that FcRL3 is expressed on a population of thymically derived T(reg) that exhibits a memory phenotype and high levels of programmed cell death-1. Purified FcRL3(+) T(reg) are less responsive to antigenic stimulation in the presence of IL-2 than their FcRL3(-) counterparts, despite intact proximal and distal IL-2 signaling as determined by phosphorylation of Stat-5 and upregulation of Bcl2. In vitro suppression assays demonstrated that FcRL3(+) T(reg) have reduced capacity to suppress the proliferation of effector T cells. These data suggest that FcRL3 expression is associated with T(reg) dysfunction that may, in turn, contribute to the loss of self-tolerance and the development of autoimmunity.

Indexed as

Antigens, CDApoptosis Regulatory ProteinsCell DifferentiationCell SeparationFlow CytometryHumansLymphocyte ActivationPhenotypePolymorphism, Single NucleotideProgrammed Cell Death 1 ReceptorReceptors, ImmunologicReverse Transcriptase Polymerase Chain ReactionSelf ToleranceSignal TransductionT-Lymphocytes, RegulatoryT-Lymphocyte SubsetsAntigens, CDApoptosis Regulatory ProteinsFCRL3 protein, humanPDCD1 protein, humanProgrammed Cell Death 1 ReceptorReceptors, Immunologic

Identifiers

PMID20190142
PMCPMC2894810
OpenAlexW1857670989

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.