Reprogramming of T cells to natural killer-like cells upon Bcl11b deletion.

Reprogramming of T cells to natural killer-like cells upon Bcl11b deletion.
复制标题

DOI:
10.1126/science.1188063
复制
发表时间:
2010-07-02
期刊:
Science (New York, N.Y.)
影响因子:
--
通讯作者:
Liu P
Liu P
中科院分区:
其他
文献类型:
--
作者:
Li P;Burke S;Wang J;Chen X;Ortiz M;Lee SC;Lu D;Campos L;Goulding D;Ng BL;Dougan G;Huntly B;Gottgens B;Jenkins NA;Copeland NG;Colucci F;Liu P

文献摘要

参考文献

被引文献

相似文献

T细胞在胸腺中发育,对适应性免疫至关重要。自然杀伤(NK)淋巴细胞是肿瘤监测、繁殖和防御微生物和病毒的先天免疫系统的重要组成部分。在这里,我们发现转录因子Bcl11b在所有T细胞区室中表达,并且对T谱系的发育是不可或缺的。当Bcl11b缺失时,所有发育阶段的T细胞都获得NK细胞特性,同时T细胞相关基因表达丢失或减少。这些诱导的T-to-natural killer (ITNK)细胞在形态和遗传上与传统NK细胞相似,在体外杀死肿瘤细胞,并在体内有效地阻止肿瘤转移。因此,ITNKs可能代表了细胞治疗的新细胞来源。
T cells develop in the thymus and are critical for adaptive immunity. Natural killer (NK) lymphocytes constitute an essential component of the innate immune system in tumor surveillance, reproduction and defense against microbes and viruses. Here we show that the transcription factor Bcl11b was expressed in all T cell compartments and was indispensable for T lineage development. When Bcl11b was deleted, T cells from all developmental stages acquired NK cell properties and concomitantly lost or decreased T cell–associated gene expression. These induced T-to–natural killer (ITNK) cells, which were morphologically and genetically similar to conventional NK cells, killed tumor cells in vitro and effectively prevented tumor metastasis in vivo. Therefore, ITNKs may represent a new cell source for cell-based therapies.
DOI: 10.1152/physiolgenomics.00019.2007
发表时间: 2007-09-19
影响因子: 4.6
作者:
Hameyer, Dorothe;Loonstra, Ate;Bockamp, Ernesto
通讯作者: Bockamp, Ernesto
DOI: 10.1084/jem.162.6.1745
发表时间: 1985-12-01
期刊: The Journal of experimental medicine
影响因子: --
作者:
Ljunggren HG;Kärre K
通讯作者: Kärre K
DOI: 10.1093/nar/22.6.965
发表时间: 1994-03-25
影响因子: 14.9
作者:
TUN, T;HAMAGUCHI, Y;KAWAICHI, M
通讯作者: KAWAICHI, M
DOI: 10.1073/pnas.0609692104
发表时间: 2007-02-27
影响因子: 11.1
作者:
Walzer, Thierry;Blery, Mathieu;Vivier, Eric
通讯作者: Vivier, Eric
DOI: 10.1016/s1074-7613(00)80185-5
发表时间: 2000-03-01
期刊: IMMUNITY
影响因子: 32.4
作者:
Miaw, SC;Choi, A;Ho, IC
通讯作者: Ho, IC