Schnurri-3 (KRC) interacts with c-Jun to regulate the IL-2 gene in T cells

被引:40
作者
Oukka, M [1 ]
Wein, MN [1 ]
Glimcher, LH [1 ]
机构
[1] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA
关键词
ZAS domain; coactivator; cytokines; AP-1; TCR signaling;
D O I
10.1084/jem.20030421
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The activator protein 1 (AP-1) transcription factor is a key participant in the control of T cell proliferation, cytokine production, and effector function. In the immune system, AP-1 activity is highest in T cells, suggesting that a subset of T cell-specific coactivator proteins exist to selectively potentiate AP-1 function. Here, we describe that the expression of Schnurri-3, also known as K recognition component (KRC), is induced upon T cell receptor signaling in T cells and functions to regulate the expression of the interleukin 2 (IL-2) gene. Overexpression of KRC in transformed and primary T cells leads to increased IL-2 production, whereas dominant-negative KRC, or loss of KRC protein in K RC-null mice, results in diminished IL-2 production. KRC physically associates with the c-Jun transcription factor and serves as a coactivator to augment AP-1-dependent IL-2 gene transcription.
引用
收藏
页码:15 / 24
页数:10
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