Evidence map›Paper›PMID 21763644›Full record

ArticleCellular immunology2011

T-cell specific defect in expression of the NTPDase CD39 as a biomarker for lupus.

Matthew J Loza, A Shane Anderson, Kenneth S O'Rourke, James Wood, Islam U Khan

Registry-linked trialAbstract read
In one paragraph

Article in Cellular immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07067112 (Suppressive Functions of Regulatory T Cells in Migraine), which is not on this map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 29% 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.

NCT07067112 nanot yet recruitingnot on this mapstarted 2026, after this paper: background citation

Suppressive Functions of Regulatory T Cells in Migraine

TypeinterventionalSponsorUniversity Hospital, Clermont-FerrandRan2026 to 2027Enrolled24ConditionsChronic MigraineArmsBlood sampling, questionnaire and phone call
3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. The TGF-b/SOX4 axis and ROS-driven autophagy co-mediate CD39 expression in regulatory T-cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

5 authors at 1 institution in 1 country.

Matthew J LozaCenter for Human Genomics, Wake Forest University Health Sciences, Winston-Salem, NC, USA.
A Shane Anderson
Kenneth S O'Rourke
James Wood
Islam U Khan
Wake Forest University · US

Funding

WORKER PROTECTION AGAINST AIRBORNE INFLUENZA - A PILOT STUDYM01RR007122 · NCRR · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI HUNDLEY, WILLIAM GREGORY · 1992 to 2010
$35.2M
T LYMPHOCYTE DYSFUNCTION IN LUPUS ERYTHEMATOSUSR01AR039501 · NIAMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI KHAN, ISLAM U · 1988 to 2006
$2.7M
Protein kinase A-dependent regulation of T cell accumulation in LupusR21AI070897 · NIAID · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI KHAN, ISLAM U · 2009 to 2010
$407k
NCRR NIH HHS M01 RR007122NCRR NIH HHS M01-RR07122NIAID NIH HHS R21 AI070897NIAMS NIH HHS R01 AR039501NIAMS NIH HHS R01 AR 39501
6 · The paper itself

Abstract

Regulatory T cells (T(regs)) are critical for maintenance of peripheral tolerance via suppression of T-cell responses, and absence of T(regs) results in autoimmunity. The role of aberrations in the T(reg) pool for the development of systemic lupus erythematosus (SLE, lupus) remains uncertain. T(reg)-mediated generation of adenosine, dependent on the ectonucleotidase CD39, is an important mechanism for suppression of T-cell responses. We tested whether decreases in numbers of T(regs), and specifically CD39-expressing T(regs), are associated with human lupus. We studied 15 SLE patients, six patients with rheumatoid arthritis (RA) and 24 healthy controls. T(reg) phenotypic markers, including CD39 expression, were studied by flow cytometry. Varying numbers of sorted T(regs) cells were co-cultured with responder T (T(resp)) cells, with proliferation assessed by (3)H-thymidine incorporation. The proportion of T(regs) as defined by Foxp3(+) CD25(+high) CD127(-/low) was similar in lupus and control populations. CD39-expressing T(regs) comprised 37±13% of the T(reg) population in healthy controls and 36±21% in lupus subjects using nonsteroidal immunosuppressants to control active disease, but was nearly absent in five of six lupus subjects with minimally active disease. In contrast to healthy controls and lupus subjects without the CD39 defect, in SLE subjects with the CD39 defect, adenosine-dependent T(reg)-mediated suppression was nearly absent. These results suggest that functional defects in T(regs), rather than reduced T(reg) numbers, are important for the loss of peripheral tolerance in lupus. Presentation of this defect may serve as a biomarker for untreated disease.

Indexed as

AdenosineAdultAgedAntigens, CDApyraseBiomarkersCell ProliferationCells, CulturedFlow CytometryHumansImmunosuppressive AgentsLupus Erythematosus, SystemicMiddle AgedT-LymphocytesT-Lymphocytes, RegulatoryXanthines8-(4-((2-aminoethyl)aminocarbonylmethyloxy)phenyl)-1,3-dipropylxanthineAdenosineAntigens, CDApyraseBiomarkersCD39 antigenImmunosuppressive AgentsXanthines

Identifiers

PMID21763644
PMCPMC3168146
OpenAlexW1981837724

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.