An intravascular immune response to Borrelia burgdorferi involves Kupffer cells and iNKT cells
An intravascular immune response to Borrelia burgdorferi involves Kupffer cells and iNKT cells
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DOI：
10.1038/ni.1855
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发表时间：
2010-04-01
影响因子：
30.5
通讯作者：
Kubes, Paul
中科院分区：
文献类型：
--
作者：
Lee, Woo-Yong;Moriarty, Tara J.;Kubes, Paul
在这里，我们调查的动态肝脏血管内免疫反应的病原体相关的不变的自然杀伤T细胞（iNKT细胞）。固定化枯否细胞具有高度分支的延伸过程，可以有效地捕获血液传播的伯氏疏螺旋体，从而创建高效的监测和过滤系统。在摄入B之后。Burgdorferi、Kupffer细胞诱导趋化因子受体CXCR 3依赖性iNKT细胞聚集。Kupffer细胞和iNKT细胞通过抗原呈递分子CD 1d形成稳定的接触，这导致iNKT细胞活化。缺乏iNKT细胞导致B。burgdorferi离开血液和更有效地进入关节。B。逃避Kupffer细胞的burgdorferi进入肝实质，尽管Ito细胞应答，但仍存活。枯否细胞-iNKT细胞相互作用诱导了一种关键的血管内免疫反应，减少了B的传播。burgdorferi。
Here we investigate the dynamics of the hepatic intravascular immune response to a pathogen relevant to invariant natural killer T cells (iNKT cells). Immobilized Kupffer cells with highly ramified extended processes into multiple sinusoids could effectively capture blood-borne, disseminating Borrelia burgdorferi, creating a highly efficient surveillance and filtering system. After ingesting B. burgdorferi, Kupffer cells induced chemokine receptor CXCR3-dependent clustering of iNKT cells. Kupffer cells and iNKT cells formed stable contacts via the antigen-presenting molecule CD1d, which led to iNKT cell activation. An absence of iNKT cells caused B. burgdorferi to leave the blood and enter the joints more effectively. B. burgdorferi that escaped Kupffer cells entered the liver parenchyma and survived despite Ito cell responses. Kupffer cell-iNKT cell interactions induced a key intravascular immune response that diminished the dissemination of B. burgdorferi.