Restoring Anticancer Immune Response by Targeting Tumor-Derived Exosomes With a HSP70 Peptide Aptamer.
Fiche publication
Date publication
mars 2016
Journal
Journal of the National Cancer Institute
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BERTAUT Aurélie, Pr FUMOLEAU Pierre, Dr GARRIDO Carmen, Pr GHIRINGHELLI François, Dr GOBBO Jessica, Pr LIRUSSI Frédéric, Mr PERNET Nicolas
Tous les auteurs :
Gobbo J, Marcion G, Cordonnier M, Dias AM, Pernet N, Hammann A, Richaud S, Mjahed H, Isambert N, Clausse V, Rébé C, Bertaut A, Goussot V, Lirussi F, Ghiringhelli F, de Thonel A, Fumoleau P, Seigneuric R, Garrido C
Lien Pubmed
Résumé
Exosomes, via heat shock protein 70 (HSP70) expressed in their membrane, are able to interact with the toll-like receptor 2 (TLR2) on myeloid-derived suppressive cells (MDSCs), thereby activating them.
Mots clés
Animals, Antineoplastic Agents, pharmacology, Aptamers, Peptide, metabolism, Breast Neoplasms, drug therapy, Cell Line, Tumor, Cell Proliferation, Colonic Neoplasms, drug therapy, Exosomes, drug effects, Female, HSP70 Heat-Shock Proteins, metabolism, Humans, Interferometry, methods, Lung Neoplasms, drug therapy, Lymphocytes, Tumor-Infiltrating, immunology, Male, Mice, Mice, Inbred C57BL, Myeloid Cells, immunology, Neoplasms, Experimental, drug therapy, Ovarian Neoplasms, drug therapy, Spleen, Toll-Like Receptor 2, metabolism
Référence
J. Natl. Cancer Inst.. 2016 Mar;108(3):