Modulation of Th1 activation and inflammation by the NF-kappaB repressor Foxj1.
Modulation of Th1 activation and inflammation by the NF-kappaB repressor Foxj1.
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发表时间：
2004
期刊：
影响因子：
56.9
通讯作者：
Ling-Yun Lin;Melanie S. Spoor;Andrea J. Gerth;S. Brody;S. Peng
中科院分区：
文献类型：
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作者：
Ling-Yun Lin;Melanie S. Spoor;Andrea J. Gerth;S. Brody;S. Peng
叉头转录因子在免疫应答的调节中起关键作用。在这里，我们确定了这个家族的一个成员Foxj 1在调节T细胞活化和自身反应性中的作用。Foxj 1缺乏导致多器官系统性炎症，夸大Th 1细胞因子的产生，和自体混合淋巴细胞反应中的T细胞增殖。Foxj 1在体外抑制NF-κ B转录活性，Foxj 1缺陷型T细胞在体内具有增加的NF-κ B活性，这与Foxj 1调节IkappaB蛋白，特别是IkappaB β的能力相关。因此，Foxj 1可能通过拮抗促炎转录活性来调节炎症反应并防止自身免疫。这些结果表明，叉头基因在淋巴细胞静止的执法潜在的一般作用。
Forkhead transcription factors play key roles in the regulation of immune responses. Here, we identify a role for one member of this family, Foxj1, in the regulation of T cell activation and autoreactivity. Foxj1 deficiency resulted in multiorgan systemic inflammation, exaggerated Th1 cytokine production, and T cell proliferation in autologous mixed lymphocyte reactions. Foxj1 suppressed NF-kappaB transcription activity in vitro, and Foxj1-deficient T cells possessed increased NF-kappaB activity in vivo, correlating with the ability of Foxj1 to regulate IkappaB proteins, particularly IkappaBbeta. Thus, Foxj1 likely modulates inflammatory reactions and prevents autoimmunity by antagonizing proinflammatory transcriptional activities. These results suggest a potentially general role for forkhead genes in the enforcement of lymphocyte quiescence.