TLR2型
趋化因子
微生物学
生物
先天免疫系统
整合素αM
TLR4型
TLR9型
金黄色葡萄球菌
免疫学
吞噬体
TLR7型
Toll样受体
吞噬作用
炎症
免疫系统
细菌
生物化学
基因表达
基因
DNA甲基化
遗传学
作者
Yasuhiro Tsuda,Hitoshi Takahashi,Makiko Kobayashi,Toshiaki Hanafusa,David N. Herndon,Fujio Suzuki
出处
期刊:Immunity
[Elsevier]
日期:2004-08-01
卷期号:21 (2): 215-226
被引量:395
标识
DOI:10.1016/j.immuni.2004.07.006
摘要
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.
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