华东理工大学排名
marite
BTN3A molecules considerably improve Vγ9Vδ2T cells-bad immunotherapy in acute myeloid马航翻译
leukemia.illustrations
期刊名称： Oncoimmunology
作者： Audrey Benyamine,Aude Le Roy,Emilie Mamessier,Julie Gertner-发票管理办法
客气英文Dardenne,Daniel Olive
年份： 2016年
期号： 第10期
怎样画眉毛关键词： Acute myeloid
leukemia;aminobisphosphonate;BTN3A;immunotherapy;monoclonal antibody;γδT cells
摘要：Given their recognized ability to kill acute myeloid leukemia (AML) blasts both in vitro and in vivo,
V9V2 T cells are of growing interest in the design of new strategies of immunotherapy. We show that the Butyrophilin3A (BTN3A, CD277) subfamily is a critical determinant of V9V2 TCR-mediated recognition of human primary AML blasts ex vivo. Moreover, anti-BTN3A 20.1 agonist monoclonal antibodies (mAbs) can trigger BTN3A on AML blasts leading to further enhanced
艾迪留学V9V2 T cell-mediated killing, but this mAb had no enhancing effect upon NK cell-mediated killing. We show that monocytic differentiation of primary AML blasts accounts for their AminoBisphosphonate (N-BP)-mediated nsitization to V9V2 T cells. In addition, anti-BTN3A 20.1 mAbs could specifically nsitize resistant blasts to V9V2 T cells lysis and overcome the poor effect
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