期刊
JOURNAL OF IMMUNOLOGY
卷 184, 期 12, 页码 7040-7046出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1000012
关键词
-
类别
资金
- Australian Research Council [DP0666515]
- Australian Research Council/National Health and Medical Research Council Research Network
- Institute for the Biotechnology of Infectious Diseases
- Faculty of Science, the University of Technology, Sydney
- Australian Research Council [DP0666515] Funding Source: Australian Research Council
The P2X(7)R is highly expressed on the macrophage cell surface, and activation of infected cells by extracellular ATP has been shown to kill intracellular bacteria and parasites. Furthermore, single nucleotide polymorphisms that decrease receptor function reduce the ability of human macrophages to kill Mycobacterium tuberculosis and are associated with extrapulmonary tuberculosis. In this study, we show that macrophages from people with the 1513C (rs3751143, NM_002562.4: c. 1487A>C) loss-of-function P2X(7)R single nucleotide polymorphism are less effective in killing intracellular Toxoplasma gondii after exposure to ATP compared with macrophages from people with the 1513A wild-type allele. Supporting a P2X(7)R-specific effect on T. gondii, macrophages from P2X(7)R knockout mice (P2X(7)R(-/-)) are unable to kill T. gondii as effectively as macrophages from wild-type mice. We show that P2X(7)R-mediated T. gondii killing occurs in parallel with host cell apoptosis and is independent of NO production. The Journal of Immunology, 2010, 184: 7040-7046.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据