Restoring Anticancer Immune Response by Targeting Tumor-Derived Exosomes With a HSP70 Peptide Aptamer.

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 , Dr GOUSSOT Vincent

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

https://www.ncbi.nlm.nih.gov/pubmed/26598503

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):