Evidence map›Paper›PMID 23553415›Full record

ArticleArthritis and rheumatism2013

Patients with antineutrophil cytoplasmic antibody-associated vasculitis have defective Treg cell function exacerbated by the presence of a suppression-resistant effector cell population.

Meghan E Free, Donna O'Dell Bunch, Julie Anne McGregor, Britta E Jones, Elisabeth A Berg, Susan L Hogan, Yichun Hu, Gloria A Preston, J Charles Jennette, Ronald J Falk and 1 more

Abstract read
In one paragraph

Article in Arthritis and rheumatism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

89 citing papers in PubMed, 160 citations in OpenAlex.

  1. Article
  2. Defects in CD8bioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Can we cure vasculitis?Current opinion in immunology · 2025
    Review
  7. Reprogramming intratumoral TScience immunology · 2025
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

29 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Meghan E FreeUniversity of North Carolina, Chapel Hill, NC, USA. meghan_free@med.unc.edu
Donna O'Dell Bunch
Julie Anne McGregor
Britta E Jones
Elisabeth A Berg
Susan L Hogan
Yichun Hu
Gloria A Preston
J Charles Jennette
Ronald J Falk
Maureen A Su
University of North Carolina at Chapel Hill · US

Funding

Translation of Knowledge on the Pathogenesis of ANCA Disease into NovelP01DK058335 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI NACHMAN, PATRICK H · 2000 to 2019
$25.9M
RENAL EPIDEMIOLOGY TRAINING PROGRAMT32DK007750 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FALK, RONALD J · 1999 to 2022
$5.5M
Autoimmune mechanisms in a novel Aire-deficient model of peripheral neuropathyR01NS079683 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SU, MAUREEN A · 2013 to 2017
$1.8M
Howard Hughes Medical InstituteNCI NIH HHS P30-CA-06086NIDDK NIH HHS 2P01-DK-058335-13NIDDK NIH HHS P01 DK058335NIDDK NIH HHS T32 DK007750NINDS NIH HHS R01 NS079683
6 · The paper itself

Abstract

objectiveThe development of pathogenic antineutrophil cytoplasmic antibodies (ANCAs) can result in systemic small vessel vasculitis. However, the breakdown in immune tolerance that results in the induction and persistence of ANCAs is not well understood. We undertook this study to test our hypothesis that abnormal T cell regulation is central to disease pathogenesis in patients with ANCA-associated vasculitis (AAV).

methodsPeripheral blood samples were obtained from 62 patients with AAV and 19 healthy controls for flow cytometric analysis of CD4+ T cell populations. Functional T cell studies were performed with fluorescence-activated cell sorted CD4+ T cell populations stimulated with anti-CD3/anti-CD28.

resultsWe demonstrated two separate abnormalities in T cell regulation in patients with AAV. First, we showed that the Treg cell frequency was increased in the peripheral blood of patients with active disease, but Treg cells from patients with AAV had decreased suppressive function. Treg cells from patients with active disease disproportionately used a FoxP3 isoform lacking exon 2, which might alter Treg cell function. Second, we identified a CD4+ T cell population with increased frequency that was resistant to Treg cell suppression, produced proinflammatory cytokines, and was antigen experienced.

conclusionAAV is associated with disruption of the suppressive Treg cell network and with increased frequency of a distinct proinflammatory effector T cell subset that comprises the majority of peripheral CD4+ T cells.

Indexed as

AdolescentAdultAgedAged, 80 and overAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisCase-Control StudiesCD4-Positive T-LymphocytesFemaleFlow CytometryForkhead Transcription FactorsHumansImmune ToleranceMaleMiddle AgedProtein IsoformsT-Lymphocytes, RegulatoryForkhead Transcription FactorsFOXP3 protein, humanProtein Isoforms

Identifiers

PMID23553415
PMCPMC3717615
OpenAlexW1691880693

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.