期刊
NATURE COMMUNICATIONS
卷 7, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms12242
关键词
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资金
- Fondation contre le Cancer (Belgium) [2010-175]
- Fonds de la Recherche Scientifique Medicale-FRSM (Belgium) [3.4514.12]
- Belgian Programme on Interuniversity Poles of Attraction [P7/39]
- Fonds de la Recherche Scientifique (F.R.S.)-FNRS (Belgium) [7.4646.09, 7.4614.11, 7.4506.13]
- BELSPO agency [IAP-7/ 38]
- F.R.S.-FNRS
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.
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