Mechanism of fate desicion between immune regulation and immune aggravation

ikb家族蛋白IkB-zeta位于细胞核内，控制NF-kB靶基因的表达。IkB-zeta缺陷（KO）小鼠随年龄增长引起自身免疫性样干燥综合征。因此，我们假设KO小鼠在抑制调节性T细胞（Treg）的能力、稳定性或产生方面存在问题。我们发现，与对照小鼠相比，KO小鼠的调节性T细胞（Tregs）的抑制能力较弱。我们还发现Tregs的稳定性在对照组和KO小鼠之间具有可比性。此外，IkB-zeta对treg的命运决定起着举足轻重的作用。

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.