Evidence map›Paper›PMID 27447355›Full record

ArticleNature communications2016

A major secretory defect of tumour-infiltrating T lymphocytes due to galectin impairing LFA-1-mediated synapse completion.

Anne-Elisabeth Petit, Nathalie Demotte, Benoît Scheid, Claude Wildmann, René Bigirimana, Monica Gordon-Alonso, Javier Carrasco, Salvatore Valitutti, Danièle Godelaine, Pierre van der Bruggen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

48 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
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  3. Galectin-9 binding to HLA-DR in dendritic cells controls immune synapse formation and T cell proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

10 authors at 6 institutions in 2 countries.

Anne-Elisabeth PetitLudwig Institute for Cancer Research, WELBIO and de Duve Institute, Université catholique de Louvain, B-1200 Brussels, Belgium.
Nathalie DemotteLudwig Institute for Cancer Research, WELBIO and de Duve Institute, Université catholique de Louvain, B-1200 Brussels, Belgium.
Benoît ScheidTIPs, Université Libre de Bruxelles, B-1050 Brussels, Belgium.
Claude WildmannLudwig Institute for Cancer Research, WELBIO and de Duve Institute, Université catholique de Louvain, B-1200 Brussels, Belgium.
René BigirimanaLudwig Institute for Cancer Research, WELBIO and de Duve Institute, Université catholique de Louvain, B-1200 Brussels, Belgium.
Monica Gordon-AlonsoLudwig Institute for Cancer Research, WELBIO and de Duve Institute, Université catholique de Louvain, B-1200 Brussels, Belgium.
Javier CarrascoDepartment of Oncology, Grand Hôpital de Charleroi, B-6000 Charleroi, Belgium.
Salvatore ValituttiINSERM, UMR 1043, Centre de Physiopathologie de Toulouse Purpan, F-31024 Toulouse, France.
Danièle GodelaineLudwig Institute for Cancer Research, WELBIO and de Duve Institute, Université catholique de Louvain, B-1200 Brussels, Belgium.
Pierre van der BruggenLudwig Institute for Cancer Research, WELBIO and de Duve Institute, Université catholique de Louvain, B-1200 Brussels, Belgium.
Walloon Excellence in Lifesciences and Biotechnology · BEde Duve Institute · BEGrand Charleroi Hospital · BEInserm · FRLudwig Cancer Research · BEUniversité Libre de Bruxelles · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Surface galectin has been shown to contribute to dysfunctions of human tumour-infiltrating lymphocytes (TILs). We show here that galectin-covered CD8 TILs produce normal amounts of intracellular cytokines, but fail to secrete them because of defective actin rearrangements at the synapse. The non-secreting TILs also display reduced adhesion to their targets, together with defective LFA-1 recruitment and activation at the synapse. These defects are relieved by releasing surface galectin. As mild LFA-1 blockade on normal blood T cells emulate the defects of galectin-covered TILs, we conclude that galectin prevents the formation of a functional secretory synapse by preventing optimal LFA-1 triggering. Our results highlight a major secretory defect of TILs that is not revealed by widely used intracellular cytokine immunomonitoring assays. They also provide additional insights into the T-cell response, by showing that different thresholds of LFA-1 triggering are required to promote the intracellular production of cytokines and their secretion.

Indexed as

GalectinsAmino SugarsCell AdhesionCell LineCytokinesHumansImmunological SynapsesLymphocyte Function-Associated Antigen-1Lymphocytes, Tumor-InfiltratingReceptors, Antigen, T-CellAmino SugarsCytokinesGalectinsLymphocyte Function-Associated Antigen-1N-acetyllactosamineReceptors, Antigen, T-Cell

Identifiers

PMID27447355
PMCPMC4961845
OpenAlexW2492596306

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.