Evidence map›Paper›PMID 22566687›Full record

ArticleMolecular and cellular biology2012

Role of LAT in the granule-mediated cytotoxicity of CD8 T cells.

Chih-wen Ou-Yang, Minghua Zhu, Deirdre M Fuller, Sarah A Sullivan, Mariana I Chuck, Sarah Ogden, Qi-Jing Li, Weiguo Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

  1. Tryptophan potentiates CD8Journal for immunotherapy of cancer · 2021
    Article
  2. Article
  3. LRCH1 deficiency enhances LAT signalosome formation and CD8Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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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

8 authors at 1 institution in 1 country.

Chih-wen Ou-YangDepartment of Immunology, Duke University Medical Center, Durham, North Carolina, USA.
Minghua Zhu
Deirdre M Fuller
Sarah A Sullivan
Mariana I Chuck
Sarah Ogden
Qi-Jing Li
Weiguo Zhang
Duke Medical Center · US

Funding

Analysis of adaptor protein (LAT) in TCR signalingR01AI048674 · NIAID · DUKE UNIVERSITY · PI ZHANG, WEIGUO · 2001 to 2011
$3.5M
Regulatory mechanisms of miR-19b, a novel mediator of T cell autoimmunityR01AI091878 · NIAID · DUKE UNIVERSITY · PI LI, QIJING · 2012 to 2016
$1.8M
Adaptor molecules in lymphocyte signalingR01AI056156 · NIAID · DUKE UNIVERSITY · PI ZHANG, WEIGUO · 2003 to 2007
$1.5M
Analysis of adaptor protein (LAT) in TCR signalingR56AI048674 · NIAID · DUKE UNIVERSITY · PI ZHANG, WEIGUO · 2012 to 2012
$385k
Adaptor molecules in lymphocyte signalingR56AI056156 · NIAID · DUKE UNIVERSITY · PI ZHANG, WEIGUO · 2010 to 2010
$382k
NIAID NIH HHS AI048674NIAID NIH HHS AI056156NIAID NIH HHS R01 AI048674NIAID NIH HHS R01 AI056156NIAID NIH HHS R01 AI091878NIAID NIH HHS R56 AI048674NIAID NIH HHS R56 AI056156
6 · The paper itself

Abstract

Linker for activation of T cells (LAT) is a transmembrane adaptor protein that is essential to bridge T cell receptor (TCR) engagement to downstream signaling events. The indispensable role of LAT in thymocyte development and T cell activation has been well characterized; however, the function of LAT in cytotoxic-T-lymphocyte (CTL) cytotoxicity remains unknown. We show here that LAT-deficient CTLs failed to upregulate FasL and produce gamma interferon after engagement with target cells and had impaired granule-mediated killing. We further dissected the effect of the LAT deletion on each step of granule exocytosis. LAT deficiency led to altered synapse formation, subsequently causing unstable T cell-antigen-presenting cell (APC) conjugates. Microtubule organizing center polarization and granule reorientation were also impaired by LAT deficiency, leading to reduced granule delivery. Despite these defects, granule release was still observed in LAT-deficient CTLs due to residual calcium flux and phospholipase C (PLC) activity. Our data demonstrated that LAT-mediated signaling intricately regulates CTL cytotoxicity at multiple steps.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCalcium SignalingCD8-Positive T-LymphocytesCytotoxicity, ImmunologicExocytosisFas Ligand ProteinImmunological SynapsesInterferon-gammaMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicPhosphoproteinsReceptors, Antigen, T-CellAdaptor Proteins, Signal TransducingFas Ligand ProteinFasl protein, mouseInterferon-gammaLat protein, mouseMembrane ProteinsPhosphoproteinsReceptors, Antigen, T-Cell

Identifiers

PMID22566687
PMCPMC3416195
OpenAlexW2161369036

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.