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


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-07-22

AUTHORS

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

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. More... »

PAGES

12242

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms12242

DOI

http://dx.doi.org/10.1038/ncomms12242

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1018296427

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27447355


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