Evidence map›Paper›PMID 10449525›Full record

ArticleThe Journal of experimental medicine1999

Antigen-specific signaling by a soluble, dimeric peptide/major histocompatibility complex class II/Fc chimera leading to T helper cell type 2 differentiation.

S Casares, C S Zong, D L Radu, A Miller, C A Bona, T D Brumeanu

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-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

19 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Signaling clusters in the cell membrane.Current opinion in cell biology · 2011
    Review
  10. T cell receptor triggering by force.Trends in immunology · 2010
    Article
  11. Article
  12. The receptor deformation model of TCR triggering.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2008
    Article
  13. Article
  14. Multimerized T cell epitopes protect from experimental autoimmune diabetes by inducing dominant tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  15. Article
  16. Article
  17. Soluble peptide-MHC monomers cause activation of CD8+ T cells through transfer of the peptide to T cell MHC molecules.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  18. Article
  19. 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

6 authors at 1 institution in 1 country.

S CasaresDepartment of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA.
C S Zong
D L Radu
A Miller
C A Bona
T D Brumeanu
Icahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interaction between a T cell receptor (TCR) and various ligands, i.e. , anti-TCR antibodies, superantigens, peptides, or altered peptide ligands in the context of major histocompatibility complex (MHC) molecules can trigger different T helper cell (Th) effector functions. Herein, we studied the T cell response induced by a soluble, dimeric peptide/MHC class II chimera, namely hemagglutinin (HA)110-120/I-E(d)alphabeta/Fcgamma2a (DEF). We have previously demonstrated that the soluble DEF molecule binds stably and specifically to HA110-120-specific TCRs expressed by a T cell hybridoma. Administration of DEF in vivo induced differentiation of resting and activated peptide-specific T cells toward a Th2 response, as indicated by the increase of interleukin (IL)-4, IL-10, and specific immunoglobulin (Ig)G1 antibodies and decrease of IL-2, specific IgG2a antibodies, and cytotoxic T lymphocyte activity. In contrast to HA110-120 peptide presented by the DEF molecule to T cells, the nominal synthetic peptide induced a predominant Th1 response, and the PR8 virus-derived HA110-120 peptides induced a mixed Th1/Th2 response. Independent of antigen processing, soluble DEF was almost 2 logs more potent in stimulating cognate T cells than the nominal peptide. Polarization of cognate T cells toward the Th2 response occurred upon interaction of soluble DEF with TCR and CD4 molecules followed by early activation of p56(lck) and ZAP-70 tyrosine kinases, and negative signaling of the signal transducer and activator of transcription (STAT)4 pathway of Th1 differentiation. DEF-like molecules may provide a new tool to study the mechanisms of signaling toward Th2 differentiation and may also provide a potential immunotherapeutic approach to modulate autoreactive T cells toward protective Th2 immune responses.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell DifferentiationDimerizationDNA-Binding ProteinsHemagglutininsHistocompatibility Antigens Class IIImmunoglobulin Fc FragmentsInterleukin-10Interleukin-2Interleukin-4Lymphocyte ActivationMiceMice, Inbred BALB CMice, TransgenicOligopeptidesDNA-Binding ProteinsHemagglutininsHistocompatibility Antigens Class IIImmunoglobulin Fc FragmentsInterleukin-10Interleukin-2Interleukin-4OligopeptidesPeptide FragmentsReceptors, Antigen, T-CellRecombinant Fusion ProteinsStat4 protein, mouseSTAT4 Transcription FactorTrans-Activators

Identifiers

PMID10449525
PMCPMC2195598
OpenAlexW2045747915

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.