Rheumatoid arthritis and function, gene expression and gene polymorphism of tristetraprolin.

三四脯氨酸（TTP）是使TNF α mRNA不稳定并抑制TNF α产生的细胞内蛋白。我们的目的是分析TTP在类风湿关节炎（RA）中的作用1。将TTP基因导入人T细胞系导致TNFα mRNA减少。对PHA刺激的反应也降低. RA患者滑膜组织中TTP、TIA-1和HuR基因表达与血清CRP水平无明显相关性。然而，重要的关系。TIA-1和HuR基因表达. RA患者外周血单个核细胞（PBMC）TNF α、TIA-1、TIA-1/HuR基因表达高于对照组，TTP、HuR、TTP/TNF α、TTP/HuR基因表达低于对照组。引入英夫利西单抗后TTP/HuR降低。对照组和RA患者接受英夫利西单抗治疗后，TIA-1和TNFα、TTP和TIA-1的表达均显著相关。英夫利西单抗治疗前TIA-1/HuR在英夫利西单抗有效患者中有升高的趋势. TTP基因启动子区SNP GG基因型的RA患者比AG或AA患者的发病年龄更早，他们也有更高的可能性引入英夫利昔单抗. TTP转基因小鼠比对照组对胶原诱导的关节炎有更强的抵抗力。

Tristetraproline (TTP) is an intracellular protein that destabilizes TNFa.mRNA and suppresses TNF α production. We aimed to analyze the role of TTP in rheumatoid arthritis (RA)1. Introduction of the TTP gene into a Human T cell line resulted in reduction of the TNFα mRNA. Response to PHA stimulation was also decreased.2. No significant relationship was observed between the expressions of TTP, TIA-1 or HuR gene, and serum CRP in synovial tissues from patients with RA. However, significant relationship between. gene expressions of TIA-1 and HuR was found.3. Gene expressions of TNFa, TIA-1, TIA-1/HuR were higher and TTP, HuR, TTP/TNFa, TTP/HuR lower in peripheral blood mononuclear cells (PBMC) of RA patients than those from controls. TTP/HuR decreased after introduction of Infliximab. Significant relationships were observed between expression of TIA-1 and TNFα, and TTP and TIA-1 in controls and RA patients after Infliximab treatment. TIA-1/HuR before Infliximab therapy tended to be higher in Infliximab effective patients.4. RA patients with genotype GG of a SNP in the promoter region of the TTP gene tended to have an earlier age of onset than those with AG or AA.They also had a higher probability of having Infliximab introduced.5. TTP transgenic mice tended to be more resistant to collagen induced arthritis than controls.