BCL6公司
生物
转录因子
效应器
细胞生物学
细胞毒性T细胞
谱系(遗传)
细胞分化
T细胞
免疫学
B细胞
卵泡期
遗传学
免疫系统
基因
生发中心
抗体
体外
作者
Roza Nurieva,Yeonseok Chung,Gustavo Martínez,Xuexian O. Yang,Shinya Tanaka,Tatyana D. Matskevitch,Yi Hong Wang,Chen Dong
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2009-08-21
卷期号:325 (5943): 1001-1005
被引量:1300
标识
DOI:10.1126/science.1176676
摘要
T Follicular Helper Cell Differentiation When B cells respond to an infection, they often require help from CD4 + T cells to mount a proper response. It is thought that a subset of CD4 + effector T cells, called T follicular helper cells (T FH ), performs this function. Several subsets of effector CD4 + T cells arise, depending on the type of infection, which have distinct transcriptional programs driving their differentiation. Whether this is also the case for T FH cells has not been clear (see the Perspective by Awasthi and Kuchroo ). Nurieva et al. (p. 1001 , published online 23 July) and Johnston et al. (p. 1006 ; published online 16 July) now demonstrate that the transcription factor Bcl6 is both necessary and sufficient for T FH differentiation and subsequent B cell–mediated immunity, suggesting that it is a master regulator of this lineage. Johnston et al. also show that expression of Bcl6 and the transcription factor, Blimp-1, are reciprocally regulated in T FH cells and that, when ectopically expressed, Blimp-1 inhibits T FH development.
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