Evidence map›Paper›PMID 12106494›Full record

ReviewArthritis research2002

The potential of human regulatory T cells generated ex vivo as a treatment for lupus and other chronic inflammatory diseases.

David A Horwitz, J Dixon Gray, Song Guo Zheng

Open access · diamondAbstract readEditorialReview
In one paragraph

Review in Arthritis research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-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

27 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. CD8Rheumatology and immunology research · 2021
    Review
  3. Article
  4. Crosstalk between T Helper Cell Subsets and Their Roles in Immunopathogenesis and Outcome of Polytrauma Patients.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2020
    Article
  5. Review
  6. Review
  7. A protocol for humanized synovitis mice model.American journal of clinical and experimental immunology · 2019
    Article
  8. Article
  9. Regulatory T cells and Atherosclerosis.Journal of clinical & experimental cardiology · 2012
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Higher expression of Bax in regulatory T cells increases vascular inflammation.Frontiers in bioscience : a journal and virtual library · 2008
    Article
  15. Article
  16. Regulatory T cells in renal disease.International journal of clinical and experimental medicine · 2008
    Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

David A HorwitzThe Division of Rheumatology and Immunology, Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, USA. dhorwitz@hsc.usc.edu
J Dixon Gray
Song Guo Zheng
University of Southern California · US

Funding

IMMUNOREGULATORY MECHANISMS IN THE RHEUMATIC DISEASESR01AI041768 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HORWITZ, DAVID A · 1997 to 2005
$1.6M
VIP--A MEDIATOR OF NEUROIMMUNE INTERACTIONSR01AI041786 · NIAID · RUTGERS THE STATE UNIV OF NJ NEWARK · PI GANEA, DOINA · 1998 to 2000
$168k
VIP--A MEDIATOR OF NEUROIMMUNE INTERACTIONSR21AI041786 · NIAID · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI GANEA, DOINA · 1997 to 1997
–
NIAID NIH HHS AI 41786NIAID NIH HHS R01 AI041768
6 · The paper itself

Abstract

Regulatory T cells prevent autoimmunity by suppressing the reactivity of potentially aggressive self-reactive T cells. Contact-dependent CD4+ CD25+ 'professional' suppressor cells and other cytokine-producing CD4+ and CD8+ T-cell subsets mediate this protective function. Evidence will be reviewed that T cells primed with transforming growth factor (TGF)-beta expand rapidly following restimulation. Certain CD4+ T cells become contact-dependent suppressor cells and other CD4+ and CD8+ cells become cytokine-producing regulatory cells. This effect is dependent upon a sufficient amount of IL-2 in the microenvironment to overcome the suppressive effects of TGF-beta. The adoptive transfer of these suppressor cells generated ex vivo can protect mice from developing chronic graft-versus-host disease with a lupus-like syndrome and alter the course of established disease. These data suggest that autologous T cells primed and expanded with TGF-beta have the potential to be used as a therapy for patients with systemic lupus erythematosus and other chronic inflammatory diseases. This novel adoptive immunotherapy also has the potential to prevent the rejection of allogeneic transplants.

Indexed as

ImmunotherapyAnimalsCD4-Positive T-LymphocytesCell TransplantationHumansInterleukin-2Lupus Erythematosus, SystemicLymphocyte ActivationReceptors, Interleukin-2T-Lymphocytes, RegulatoryT-Lymphocyte SubsetsTransforming Growth Factor betaInterleukin-2Receptors, Interleukin-2Transforming Growth Factor beta

Identifiers

PMID12106494
PMCPMC128930
OpenAlexW1555334455

What OpenQuestion holds

Textmetadata
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.