Evidence map›Paper›PMID 20855626›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Promoting tolerance to proteolipid protein-induced experimental autoimmune encephalomyelitis through targeting dendritic cells.

Joel N H Stern, Derin B Keskin, Zenichiro Kato, Hanspeter Waldner, Sonja Schallenberg, Ana Anderson, Harald von Boehmer, Karsten Kretschmer, Jack L Strominger

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

44 citing papers in PubMed, 71 citations in OpenAlex.

  1. Multiple sclerosis: molecular pathogenesis and therapeutic intervention.Signal transduction and targeted therapy · 2025
    Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Tolerogenic Dendritic Cell-Based Approaches in Autoimmunity.International journal of molecular sciences · 2021
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Targeting DEC-205Molecular medicine (Cambridge, Mass.) · 2018
    Article
  14. Review
  15. CLEC10A Is a Specific Marker for Human CD1cFrontiers in immunology · 2018
    Article
  16. Article
  17. Review
  18. Review
  19. Tolerogenic dendritic cells.Seminars in immunopathology · 2017
    Review
  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

9 authors at 2 institutions in 2 countries.

Joel N H SternDepartment of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA. jstern@fas.harvard.edu
Derin B Keskin
Zenichiro Kato
Hanspeter Waldner
Sonja Schallenberg
Ana Anderson
Harald von Boehmer
Karsten Kretschmer
Jack L Strominger
Harvard University · USTU Dresden · DE

Funding

MHC proteins, copolymers and peptide 15mers in EAER01AI049524 · NIAID · HARVARD UNIVERSITY · PI STROMINGER, JACK L · 2001 to 2010
$5.7M
NIAID NIH HHS AI049524NIAID NIH HHS R01 AI049524
6 · The paper itself

Abstract

In T cell-mediated autoimmune diseases, self-reactive T cells with known antigen specificity appear to be particularly promising targets for antigen-specific induction of tolerance without compromising desired protective host immune responses. Several lines of evidence suggest that delivery of antigens to antigen-presenting dendritic cells (DCs) in the steady state (i.e., to immature DCs) may represent a suitable approach to induce antigen-specific T-cell tolerance peripherally. Here, we report that anti-DEC205-mediated delivery of the self-peptide proteolipid protein (PLP)139-151 to DCs ameliorated clinical symptoms in the PLP-induced SJL model of experimental autoimmune encephalomyelitis. Splenocytes from treated mice were anergized to PLP139-151, and IL-17 secretion was markedly reduced. Moreover, we show directly, using transgenic CD4(+) Vβ6(+) TCR T cells specific for PLP139-151, that, under the conditions of the present experiments, these cells also became anergic. In addition, evidence for a CD4(+) T cell-mediated suppressor mechanism was obtained.

Indexed as

Adoptive TransferAnimalsCell LineDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansImmune ToleranceInterleukin-17MiceMice, Inbred StrainsMice, TransgenicMyelin Proteolipid ProteinPeptide FragmentsRecombinant Fusion ProteinsInterleukin-17Myelin Proteolipid Proteinmyelin proteolipid protein (139-151)Peptide FragmentsRecombinant Fusion Proteins

Identifiers

PMID20855626
PMCPMC2951396
OpenAlexW2083909742

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.