小分子热休克蛋白Hsp16.3参与介导结核分枝杆菌致巨噬细胞凋亡的研究进展  

Small Molecular Heat Shock Protein Hsp16.3 Involved in the Study of Macrophage Apoptosis induced by Mycobacterium Tuberculosis

作　　者：黄丹丹[1] HUANG Dan-dan(Preclinical School of North Sichuan Medical College,Nanchong,Sichuan Province,637007 Chin)

机构地区：[1]川北医学院基础医学院,四川南充637007

出　　处：《系统医学》2018年第3期193-195,共3页Systems Medicine

基　　金：四川省教育厅自科重点项目(13ZA0217);川北医学院博士基金项目(CBY15-QD04)

摘　　要：结核病是世界范围内亟待解决的问题之一。Hsp16.3分布于结核分枝杆菌,其可介导MTB在巨噬细胞内稳定生长,并延迟、减少巨噬细胞凋亡。该研究进展总结出在巨噬细胞凋亡过程中,Hsp16.3可通过影响LC3,miR-181a、miR-146a,TLR2与LAG3等4条可能的通路,进而减少细胞凋亡过程。此外,该研究还针对Hsp16.3提出早期分子检测、靶向药物开发、Hsp16.3疫苗研发等临床应用意见,以期为临床治疗提供帮助指导。tuberculosis is one of the problems that need to be solved in the world. Hsp16.3 is distributed in Mycobacterium tuberculosis, which can mediate the stable growth of MTB in macrophages and delay and reduce the apoptosis of macrophages. This research concluded that in the process of macrophage apoptosis, Hsp16.3 can reduce the apoptotic process by affecting four possible pathways, such as LC3, miR-181a, miR-146a, TLR2 and LAG3. In addition, we also put forward some suggestions for clinical application of Hsp16.3, such as early molecular detection, targeted drug development, Hsp16.3 vaccine research and development, so as to provide guidance for clinical treatment.

关 键 词：小分子热休克蛋白 结核分枝杆菌 巨噬细胞 凋亡 靶向治疗 

分 类 号：R392.11[医药卫生—免疫学]