Altering the specificity of NK:target cell interactions by genetic manipulation of NK receptor expression on primary mouse NK cells

被引:6
|
作者
Tran, Jimmy [1 ]
Mahmood, Sajid [1 ]
Carlyle, James R. [2 ,3 ]
Kung, Sam K. P. [1 ]
机构
[1] Univ Manitoba, Dept Immunol, Apotex Ctr, Winnipeg, MB R3E 0T5, Canada
[2] Univ Toronto, Dept Immunol, Toronto, ON M4N 3M5, Canada
[3] Sunnybrook Res Inst, Toronto, ON M4N 3M5, Canada
基金
加拿大自然科学与工程研究理事会; 加拿大健康研究院;
关键词
Lentiviral vectors; NK and immunotherapy; NATURAL-KILLER-CELLS; ANTIGEN; IDENTIFICATION; ALLOREACTIVITY; DEGRANULATION; NKR-P1B;
D O I
10.1016/j.vaccine.2010.03.013
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
A balance of signals generated via stimulatory and inhibitory NK receptors determines both target cell specificity and the outcome of NK-target cell interactions. The feasibility of introducing naturally occurring or genetically engineered chimeric NM receptors at the effector cell level may prove useful in NK cell-based immunotherapies. Here, we utilized a previously established lentiviral transduction system to over-express a model NKR-P1B inhibitory receptor on primary mouse NK cells. These genetically engineered NM cells became more sensitive to inhibitory signals delivered by target cells expressing the cognate NKR-P1B ligand, Ocil/Clr-b. This study demonstrated the utility of lentiviral vectors as a means to stably manipulate the target cell specificity of primary NM cells. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:3767 / 3772
页数:6
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