细胞凋亡
免疫系统
THP1细胞系
结核分枝杆菌
生物
巨噬细胞
程序性细胞死亡
微生物学
基因敲除
信号转导
细胞生物学
免疫学
细胞培养
肺结核
医学
体外
病理
生物化学
遗传学
作者
Jun Tang,Zhan Li,Chuan Qin
标识
DOI:10.1016/j.micpath.2015.11.028
摘要
Apoptosis was considered as one of the important host defense mechanisms against mycobacteria infection. In macrophage, the main target cell of Mycobacterium tuberculosis, apoptosis after infection could help kill the bacillus inside and process the antigens for further presentation and proper immune response. Here, we identified a role of TLR8 during the apoptosis induced by Bacillus Calmette Guérin (BCG) infection in THP-1 cells. Knockdown TLR8 further increased the apoptosis induced by BCG infection, and this enhanced apoptosis was caspase-dependent. During this process, Erk1/2, JNK and NFκB pathways were negatively affected and contributed to the enhanced apoptosis.
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