期刊
IMMUNITY
卷 21, 期 2, 页码 215-226出版社
CELL PRESS
DOI: 10.1016/j.immuni.2004.07.006
关键词
-
类别
资金
- NIAID NIH HHS [AI44218] Funding Source: Medline
Neutrophils (PMN) have been described as critical effector cells in the host's antibacterial innate immunities. However, the classification of murine PMNs remains unclear. Here, we show that in addition to normal PMN (PMN-N), there are at least two distinct subsets of PMNs (PMN-I and PMN-II) distinguished as follows: (1) cytokine and chemokine production (PMN-I, IL-12/CCL3; PMN-II, IL-10/CCL2; PMN-N, no cytokine/chemokine production), (2) macrophage activation (PMN-I, classically activated macrophages; PMN-II, alternatively activated macrophages; PMN-N, no effect on macrophage activation), (3) Toll-like receptor (TLR) expression (PMN-I, TLR2/TLR4/TLR5/ TLR8; PMN-II, TLR2/TLR4/TLR7/TLR9; PMN-N, TLR2/ TLR4/TLR9), and (4) surface antigen expression (PMN-I, CD49d(+)CD11b(-); PMN-II, CD49d(-)CD11b(+); PMN-N, CD49d(-)CD11b(-)). PMN-I was obtained from MRSA (methicillin-resistant Staphylococcus aureus)-resistant hosts, while MRSA-sensitive hosts were a source of PMN-II. PMN-N was obtained from naive mice. Anti-MRSA innate immunities might be influenced differently by these biochemically and physically distinguished PMNs. PMN-N may convert to PMN-I or PMN-II in response to host circumstance.
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