Evidence map›Paper›PMID 19130025›Full record

ReviewResults and problems in cell differentiation2010

Prospects for antigen-specific tolerance based therapies for the treatment of multiple sclerosis.

Danielle M Turley, Stephen D Miller

Open access · greenAbstract readReview
In one paragraph

Review in Results and problems in cell differentiation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
  2. Article
  3. Multiple sclerosis: molecular pathogenesis and therapeutic intervention.Signal transduction and targeted therapy · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Immune Modulation and Prevention of Autoimmune Disease by Repeated Sequences from Parasites Linked to Self Antigens.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016
    Article
  13. Restoring immune tolerance in neuromyelitis optica: Part I.Neurology(R) neuroimmunology & neuroinflammation · 2016
    Review
  14. Emerging immunopharmacological targets in multiple sclerosis.Journal of the neurological sciences · 2015
    Review
  15. Article
  16. Review
  17. Article
  18. Engineering antigens for in situ erythrocyte binding induces T-cell deletion.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  19. The inside story of dendritic cell immunotherapy.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2012
    Article
  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

2 authors at 1 institution in 1 country.

Danielle M TurleyDepartment of Microbiology-Immunology and the Interdepartmental Immunobiology Center, Northwestern University Medical School, Tarry 6-718, 303 E. Chicago Ave, Chicago, IL 60611, USA.
Stephen D Miller
Northwestern University · US

Funding

IMMUNOREGULATION AND PATHOLOGY OF CHRONIC-RELAPSING EAER01NS026543 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1988 to 2016
$5.0M
PATHOGENESIS AND IMMUNOREGULATION OF PLP-INDUCED R-EAER01NS030871 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1993 to 2010
$3.4M
B7/CD28 MEDIATED COSTIMULATION IN THE PATHOLOGY OF R EAER01NS034819 · NINDS · NORTHWESTERN UNIVERSITY · PI MILLER, STEPHEN D · 1996 to 2003
$1.4M
Mechanisms of CD4+CD25+ T Regulatory Cells in EAER01NS048411 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 2005 to 2008
$1.3M
NINDS NIH HHS R01 NS026543NINDS NIH HHS R01 NS030871NINDS NIH HHS R01 NS034819NINDS NIH HHS R01 NS048411
6 · The paper itself

Abstract

A primary focus in autoimmunity is the breakdown of central and peripheral tolerance resulting in the survival and eventual activation of autoreactive T cells. As CD4(+) T cells are key contributors to the underlying pathogenic mechanisms responsible for onset and progression of most autoimmune diseases, they are a logical target for therapeutic strategies. One method for restoring self-tolerance is to exploit the endogenous regulatory mechanisms that govern CD4(+) T cell activation. In this review, we discuss tolerance strategies with the common goal of inducing antigen (Ag)-specific tolerance. Emphasis is given to the use of peptide-specific tolerance strategies, focusing on ethylene carbodiimide (ECDI)-peptide-coupled cells (Ag-SP) and nonmitogenic anti-CD3, which specifically target the T cell receptor (TCR) in the absence of costimulatory signals. These approaches induce a TCR signal of insufficient strength to cause CD4(+) T cell activation and instead lead to functional T cell anergy/deletion and activation of Ag-specific induced regulatory T cells (iTregs) while avoiding generalized long-term immunosuppression.

Indexed as

AnimalsAntibodies, MonoclonalAutoantigensAutoimmunityCarbodiimidesCD4-Positive T-LymphocytesEncephalomyelitis, Autoimmune, ExperimentalHumansImmunity, MucosalImmunosuppression TherapyMiceMultiple SclerosisPeptidesReceptors, Antigen, T-CellSelf ToleranceT-Lymphocytes, RegulatoryAntibodies, MonoclonalAutoantigensCarbodiimidesPeptidesReceptors, Antigen, T-Cell

Identifiers

PMID19130025
PMCPMC2901403
OpenAlexW1507805073

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.