肝星状细胞
库普弗电池
生物
细胞生物学
肝细胞学
趋化因子
肿瘤坏死因子α
内皮干细胞
单核细胞
正弦周空间
免疫学
炎症
肝细胞
内分泌学
生物化学
体外
肝脏代谢
作者
Johnny Bonnardel,Wouter T’Jonck,Djoere Gaublomme,Robin Browaeys,Charlotte Scott,Liesbet Martens,Bavo Vanneste,Sofie De Prijck,Sergei A. Nedospasov,Anna Kremer,Evelien Van Hamme,Peter Borghgraef,Wendy Toussaint,Pieter De Bleser,Inge Mannaerts,Alain Beschin,Leo A. van Grunsven,Bart N. Lambrecht,Tom Taghon,Saskia Lippens,Dirk Elewaut,Yvan Saeys,Martin Guilliams
出处
期刊:Immunity
[Elsevier]
日期:2019-10-01
卷期号:51 (4): 638-654.e9
被引量:368
标识
DOI:10.1016/j.immuni.2019.08.017
摘要
Summary
Macrophages are strongly adapted to their tissue of residence. Yet, little is known about the cell-cell interactions that imprint the tissue-specific identities of macrophages in their respective niches. Using conditional depletion of liver Kupffer cells, we traced the developmental stages of monocytes differentiating into Kupffer cells and mapped the cellular interactions imprinting the Kupffer cell identity. Kupffer cell loss induced tumor necrosis factor (TNF)- and interleukin-1 (IL-1) receptor-dependent activation of stellate cells and endothelial cells, resulting in the transient production of chemokines and adhesion molecules orchestrating monocyte engraftment. Engrafted circulating monocytes transmigrated into the perisinusoidal space and acquired the liver-associated transcription factors inhibitor of DNA 3 (ID3) and liver X receptor-α (LXR-α). Coordinated interactions with hepatocytes induced ID3 expression, whereas endothelial cells and stellate cells induced LXR-α via a synergistic NOTCH-BMP pathway. This study shows that the Kupffer cell niche is composed of stellate cells, hepatocytes, and endothelial cells that together imprint the liver-specific macrophage identity.
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