NKG2D公司
细胞生物学
微泡
T细胞
生物
细胞生长
树突状细胞
外体
效应器
细胞
免疫学
免疫系统
细胞毒性T细胞
体外
生物化学
小RNA
基因
作者
Sophie Viaud,Magali Terme,Caroline Flament,Julien Taı̈eb,Fabrice André,Sophie Novault,Bernard Escudier,Caroline Robert,Sophie Caillat‐Zucman,Thomas Tursz,Laurence Zitvogel,Nathalie Chaput
出处
期刊:PLOS ONE
[Public Library of Science]
日期:2009-03-24
卷期号:4 (3): e4942-e4942
被引量:402
标识
DOI:10.1371/journal.pone.0004942
摘要
Dendritic cell (DC) derived-exosomes (Dex) are nanomeric vesicles harboring functional MHC/peptide complexes promoting T cell-dependent tumor rejection. In the first Phase I trial using peptide-pulsed Dex, the observation of clinical regressions in the absence of T cell responses prompted the search for alternate effector mechanisms. Mouse studies unraveled the bioactivity of Dex on NK cells. Indeed, Dex promoted an IL-15Ralpha- and NKG2D-dependent NK cell proliferation and activation respectively, resulting in anti-metastatic effects mediated by NK1.1(+) cells. In humans, Dex express functional IL-15Ralpha which allow proliferation and IFNgamma secretion by NK cells. In contrast to immature DC, human Dex harbor NKG2D ligands on their surface leading to a direct engagement of NKG2D and NK cell activation ex vivo. In our phase I clinical trial, we highlight the capacity of Dex based-vaccines to restore the number and NKG2D-dependent function of NK cells in 7/14 patients. Altogether, these data provide a mechanistic explanation on how Dex may stimulate non MHC restricted-anti-tumor effectors and induce tumor regression in vivo.
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