颗粒溶素
生物
穿孔素
细胞溶解
颗粒酶
细胞毒性T细胞
微生物学
细胞生物学
细胞内
NKG2D公司
免疫系统
细胞内寄生虫
免疫学
CD8型
体外
生物化学
作者
Cuihua Lu,Ting‐Shu Wu,Ya-Jing Hsu,Chi-Jen Chang,Chwan-Fwu Lin,Ju‐Hsin Chia,Tsu‐Lan Wu,Tzu Ting Huang,Jan Martel,David M. Ojcius,John Ding‐E Young,Hsin–Chih Lai
标识
DOI:10.1189/jlb.4a0713-363rr
摘要
Although the mechanisms underlying the cytotoxic effect of NK cells on tumor cells and intracellular bacteria have been studied extensively, it remains unclear how these cells kill extracellular bacterial pathogens. In this study, we examine how human NK cells kill Mycobacterium kansasii and M.tb. The underlying mechanism is contact dependent and requires two cytolytic proteins: perforin and granulysin. Mycobacteria induce enhanced expression of the cytolytic proteins via activation of the NKG2D/NCR cell-surface receptors and intracellular signaling pathways involving ERK, JNK, and p38 MAPKs. These results suggest that NK cells use similar cellular mechanisms to kill both bacterial pathogens and target host cells. This report reveals a novel role for NK cells, perforin, and granulysin in killing mycobacteria and highlights a potential alternative defense mechanism that the immune system can use against mycobacterial infection.
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