Evidence map›Paper›PMID 22935418›Full record

ArticleBiochemical and biophysical research communications2012

Engagement of T-cell antigen receptor and CD4/CD8 co-receptors induces prolonged STAT activation through autocrine/paracrine stimulation in human primary T cells.

Fu-Yu Chueh, Chao-Lan Yu

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Intracellular KScientific reports · 2019
    Article
  5. Reporters of TCR signaling identify arthritogenic T cells in murine and human autoimmune arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Biomaterial Strategies for Immunomodulation.Annual review of biomedical engineering · 2015
    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

2 authors at 1 institution in 1 country.

Fu-Yu ChuehDepartment of Microbiology and Immunology, H.M. Bligh Cancer Research Laboratories, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, USA.
Chao-Lan Yu
Rosalind Franklin University of Medicine and Science · US

Funding

SOCS: Its Regulation and Role in OncogenesisR01CA107210 · NCI · VANDERBILT UNIVERSITY · PI YU, CHAO-LAN · 2006 to 2010
$1.2M
NCI NIH HHS R01 CA107210
6 · The paper itself

Abstract

Signal transducer and activator of transcription (STAT) proteins are key signaling molecules in response to cytokines and in regulating T cell biology. However, there are contradicting reports on whether STAT is involved in T-cell antigen receptor (TCR) signaling. To better define the role of STAT in TCR signaling, we activated the CD4/CD8-associated Lck kinase by co-crosslinking TCR and CD4/CD8 co-receptors in human peripheral blood T cells. Sequential STAT1, STAT3 and STAT5 activation was observed 1 h after TCR stimulation suggesting that STAT proteins are not the immediate targets in the TCR complex. We further identified interferon-γ as the key cytokine in STAT1 activation upon TCR engagement. In contrast to transient STAT activation in cytokine response, this autocrine/paracrine-induced STAT activation was sustained. It correlated with the absence of two suppressors of cytokine signaling (SOCS) proteins, SOCS3 and cytokine-inducible SH2 containing protein that are negative feedback regulators of STAT signaling. Moreover, enforced expression of SOCS3 inhibited tyrosine phosphorylation of zeta-associated protein kinase of 70 kD in TCR-stimulated human Jurkat T cells. This is the first report demonstrating delayed and prolonged STAT activation coordinated with the loss of SOCS expression in human primary T cells after co-crosslinking of TCR and CD4/CD8 co-receptors.

Indexed as

Autocrine CommunicationCD4 AntigensCD8 AntigensGene ExpressionHumansJurkat CellsLymphocyte Specific Protein Tyrosine Kinase p56(lck)Paracrine CommunicationPhosphorylationReceptors, Antigen, T-CellSTAT1 Transcription FactorSTAT3 Transcription FactorSTAT5 Transcription FactorSTAT Transcription FactorsSuppressor of Cytokine Signaling ProteinsT-LymphocytesCD4 AntigensCD8 AntigensLymphocyte Specific Protein Tyrosine Kinase p56(lck)Receptors, Antigen, T-CellSTAT1 protein, humanSTAT1 Transcription FactorSTAT3 protein, humanSTAT3 Transcription FactorSTAT5 Transcription FactorSTAT Transcription FactorsSuppressor of Cytokine Signaling ProteinsTyrosine

Identifiers

PMID22935418
PMCPMC3597241
OpenAlexW2094061652

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.