Mechanism of fate desicion between immune regulation and immune aggravation

IKB-家族蛋白、IKB-Zeta定位于核内，控制着核转录因子-kB靶基因的表达。IKB-Zeta基因缺陷(KO)小鼠随着年龄的增长引起自身免疫性干燥综合征，因此我们假设KO小鼠在抑制能力、稳定性或调节性T细胞(Treg)的生成方面存在问题。我们还发现，Tregs的稳定性在对照组和KO小鼠之间是相似的。此外，IKB-Zeta在Tregs命运注定中扮演着举足轻重的角色。

IkB-family protein, IkB-zeta located into nuclear, and control NF-kB target gene expression. IkB-zeta deficient (KO) mice caused autoimmune like sjogren's syndrome with age.Thus, we hypothesis that KO mice have problem about the suppressor ability, stability or generation of regulatory T cells (Treg).We found that regulatory T cells (Tregs) from KO mice has less suppression ability compared with control mice. We also found that stability of Tregs were comparable between control and KO mice. In addition, IkB-zeta plays an pivotal role for Tregs fate desition.