Evidence map›Paper›PMID 15557350›Full record

ArticleThe Journal of experimental medicine2004

Functional reprogramming of the primary immune response by T cell receptor antagonism.

Dipica Haribhai, Brandon Edwards, Mary L Williams, Calvin B Williams

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

4 authors.

Dipica HaribhaiDepartment of Pediatrics, Medical College of Wisconsin, 8701 Watertown Plank Rd., Milwaukee, WI 53226, USA.
Brandon Edwards
Mary L Williams
Calvin B Williams

Funding

SELECTION AND SURVIVAL OF T LYMPHOCYTESR01AI047154 · NIAID · WASHINGTON UNIVERSITY · PI WILLIAMS, CALVIN B · 2000 to 2004
$1.5M
NIAID NIH HHS R01 AI047154
6 · The paper itself

Abstract

The T cell receptor must translate modest, quantitative differences in ligand binding kinetics into the qualitatively distinct signals used to determine cell fate. Here, we use mice that express an endogenous T cell receptor (TCR) antagonist and an adoptive transfer system to examine the influence of TCR signal quality on the development of effector function. We show that activation of antigen-specific T cells in the presence of an antagonist results in a functional reprogramming of the primary immune response, marked by altered T cell homing, a failure to develop effector function, and ultimately clonal elimination by apoptosis. Importantly, antagonism does not block cell division, implying that the signals promoting clonal expansion and effector differentiation are distinct.

Indexed as

Adoptive TransferAnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteCaspase 3CaspasesCD69 AntigensClonal DeletionEnzyme ActivationImmune ToleranceImmunizationImmunologic MemoryIntracellular Signaling Peptides and ProteinsLectins, C-TypeLymphocyte ActivationMembrane ProteinsAntigens, CDAntigens, Differentiation, T-Lymphocyteantigen T cell receptor, zeta chainCasp3 protein, mouseCaspase 3CaspasesCD69 AntigensIntracellular Signaling Peptides and ProteinsLectins, C-TypeMembrane ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesPtpn6 protein, mouseReceptors, Antigen, T-Cell

Identifiers

PMID15557350
PMCPMC2211957

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.