期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 106, 期 18, 页码 7642-7647出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0902761106
关键词
HV1(-/-); immunity; voltage-gated ion channel; innate immunity
资金
- National Institutes of Health [T32 HLO7572, P30-HD18655]
Granulocytes generate a respiratory burst'' of NADPH oxidase-dependent superoxide anion (O-2(-center dot)) production that is required for efficient clearance of bacterial pathogens. Hv1 mediates a voltage-gated H+ channel activity that is proposed to serve a charge-balancing role in granulocytic phagocytes such as neutrophils and eosinophils. Using mice in which the gene encoding Hv1 is replaced by beta-Geo reporter protein sequence, we show that Hv1 expression is required for measurable voltage-gated H+ current in unstimulated phagocytes. O-2(-center dot) production is substantially reduced in the absence of Hv1, suggesting that Hv1 contributes a majority of the charge compensation required for optimal NADPH oxidase activity. Despite significant reduction in superoxide production, Hv1(-/-) mice are able to clear several types of bacterial infections.
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