T helper cell fate specified by kinase-mediated interaction of T-bet with GATA-3

被引：402

作者：

Hwang, ES

Szabo, SJ

Schwartzberg, PL

Glimcher, LH

机构：

[1] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA

[3] NHGRI, NIH, Bethesda, MD 20892 USA

来源：

SCIENCE | 2005年 / 307卷 / 5708期

关键词：

D O I：

10.1126/science.1103336

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Cell Lineage specification depends on both gene activation and gene silencing, and in the differentiation of T helper progenitors to Th1 or Th2 effector cells, this requires the action of two opposing transcription factors, T-bet and GATA-3. T-bet is essential for the development of Th1 cells, and GATA-3 performs an equivalent role in Th2 development. We report that T-bet represses Th2 lineage commitment through tyrosine kinase-mediated interaction between the two transcription factors that interferes with the binding of GATA-3 to its target DNA. These results provide a novel function for tyrosine phosphorylation of a transcription factor in specifying alternate fates of a common progenitor cell.

引用

收藏

页码：430 / 433

页数：4

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