标题:Intestinal CD169(+) macrophages initiate mucosal inflammation by secreting CCL8 that recruits inflammatory monocytes
作者:Asano, Kenichi; Takahashi, Naomichi; Ushiki, Mikiko; Monya, Misa; Aihara, Fumiaki; Kuboki, Erika; Moriyama, Shigetaka; Iida, Mayumi; K 更多
作者机构:[Asano, Kenichi; Takahashi, Naomichi; Ushiki, Mikiko; Monya, Misa; Aihara, Fumiaki; Kuboki, Erika; Moriyama, Shigetaka; Iida, Mayumi; Tanaka, Masato] 更多
通讯作者:Asano, K
通讯作者地址:[Asano, K]Tokyo Univ Pharm & Life Sci, Sch Life Sci, Lab Immune Regulat, 1432-1 Horinouchi, Hachioji, Tokyo 1920392, Japan.
来源:NATURE COMMUNICATIONS
出版年:2015
卷:6
DOI:10.1038/ncomms8802
摘要:Lamina propria (LP) macrophages are constantly exposed to commensal bacteria, and are refractory to those antigens in an interleukin (IL)-10-dependent fashion. However, the mechanisms that discriminate hazardous invasion by bacteria from peaceful co-existence with them remain elusive. Here we show that CD169(+) macrophages reside not at the villus tip, but at the bottom-end of the LP microenvironment. Following mucosal injury, the CD169(+) macrophages recruit inflammatory monocytes by secreting CCL8. Selective depletion of CD169(+) macrophages or administration of neutralizing anti-CCL8 antibody ameliorates the symptoms of experimentally induced colitis in mice. Collectively, we identify an LP-resident macrophage subset that links mucosal damage and inflammatory monocyte recruitment. Our results suggest that CD169(+) macrophage-derived CCL8 serves as an emergency alert for the collapse of barrier defence, and is a promising target for the suppression of mucosal injury.
收录类别:SCIE
WOS核心被引频次:26
资源类型:期刊论文
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