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目的探讨干扰素诱导蛋白IFI 16及其Janus激酶/信号转导和转录激活因子(JAK-STAT)信号转导途径在系统性红斑狼疮(SLE)发病中的作用。方法逆转录-聚合酶链反应(RT-PCR)检测35例SLE患者和16例正常人外周血单一核细胞(PBMC)中IFI 16的表达水平。体外培养PBMC,用JAK2抑制剂AG490抑制JAK-STAT信号转导途径,再用RT-PCR检测PBMC中IFI 16的表达水平。结果与对照组比较,活动期、非活动期组IFI 16 mRNA的表达水平明显增高,差异均有统计学意义(P＜0．001)。而活动期与非活动期组比较,差异无统计学意义(P＞0．05)。在用AG490抑制JAK-STAT信号转导途径后,活动期与非活动期组PBMC中IFI 16 mRNA的表达水平均明显下降,差异均有统计学意义(P＜0．001),而正常组用药前后比较差异无统计学意义(P＞0．05)。结论IFI 16在SLE患者的异常高表达提示IFI 16基因可能为SLE的致病基因之一。
Objective To investigate the role of interferon-inducible protein IFI-16 and its Janus kinase / signal transducers and activators of transcription (JAK-STAT) signaling pathway in the pathogenesis of systemic lupus erythematosus (SLE). Methods The expression of IFI-16 in peripheral blood mononuclear cells (PBMCs) of 35 SLE patients and 16 healthy controls was detected by reverse transcription-polymerase chain reaction (RT-PCR). PBMCs were cultured in vitro, the JAK-STAT signal transduction pathway was inhibited by JAK2 inhibitor AG490, and the expression level of IFI 16 in PBMC was detected by RT-PCR. Results Compared with the control group, the expression of IFI 16 mRNA in active and inactive groups was significantly increased, with statistical significance (P <0.001). However, there was no significant difference between active and inactive groups (P> 0.05). After AG490 was used to inhibit the JAK-STAT signal transduction pathway, the expressions of IFI 16 mRNA in active and inactive PBMCs were significantly decreased, with significant differences (P <0.001), while those in normal group Before and after the difference was not statistically significant (P> 0.05). Conclusion The abnormally high expression of IFI16 in SLE patients suggests that IFI 16 gene may be one of the pathogenic genes of SLE.