Regulatory mechanism of the generation of immune response to Mycobacterium tuberculosis infection

本研究旨在探讨结核分枝杆菌与M。BCG调节感染宿主的免疫应答。研究结果表明，M.与细菌毒力高度相关的结核杆菌基因组分别通过促进钙蛋白酶和半胱天冬酶-1的活化而参与IL-1α、IL-1β和IL-18的产生。此外，分枝杆菌PPE 37蛋白可能有助于抑制感染巨噬细胞产生IL-6和TNF-α。此外，已经显示PD-1信号通路是抑制对M的超免疫应答所必需的。肺结核感染。另一方面，可以肯定的是，卡介苗接种的效果是通过信号通路的障碍而增强的。

This study was carried out to find out the molecular mechanism as to how Mycobacterium tuberculosis and M. bovis BCG regulate the immune response in infected host. The research revealed that the RD1 locus in the M. tuberculosis genome, which is highly implicated in bacterial virulence, is involved in the production of IL-1α, IL-1βand IL-18 by promoting the activation of calpain and caspase-1, respectively. In addition, it is probable that mycobacterial PPE37 protein contributes to the inhibition of IL-6 and TNF-αproduction from infected macrophages. Moreover, it has been shown that the PD-1 signal pathway is required for the suppression of hyper-immune response to M. tuberculosis infection. On the other hand, it is certain that the efficacy of BCG vaccination is enhanced by the impediment of signal pathway.