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组织驻留型CD169(+)巨噬细胞构成抵御疟原虫感染的关键防线。

Tissue-Resident CD169(+) Macrophages Form a Crucial Front Line against Plasmodium Infection.

作者信息

Gupta Pravesh, Lai Si Min, Sheng Jianpeng, Tetlak Piotr, Balachander Akhila, Claser Carla, Renia Laurent, Karjalainen Klaus, Ruedl Christiane

机构信息

Nanyang Technological University, School of Biological Sciences, 60 Nanyang Drive, Singapore 637551, Singapore.

Nanyang Technological University, School of Biological Sciences, 60 Nanyang Drive, Singapore 637551, Singapore; Singapore Immunology Network, Agency for Science, Technology and Research (A(∗)STAR), 8A Biomedical Grove, Singapore 138648, Singapore.

出版信息

Cell Rep. 2016 Aug 9;16(6):1749-1761. doi: 10.1016/j.celrep.2016.07.010. Epub 2016 Jul 28.

DOI:10.1016/j.celrep.2016.07.010
PMID:27477286
Abstract

Tissue macrophages exhibit diverse functions, ranging from the maintenance of tissue homeostasis, including clearance of senescent erythrocytes and cell debris, to modulation of inflammation and immunity. Their contribution to the control of blood-stage malaria remains unclear. Here, we show that in the absence of tissue-resident CD169(+) macrophages, Plasmodium berghei ANKA (PbA) infection results in significantly increased parasite sequestration, leading to vascular occlusion and leakage and augmented tissue deposition of the malarial pigment hemozoin. This leads to widespread tissue damage culminating in multiple organ inflammation. Thus, the capacity of CD169(+) macrophages to contain the parasite burden and its sequestration into different tissues and to limit infection-induced inflammation is crucial to mitigating Plasmodium infection and pathogenesis.

摘要

组织巨噬细胞具有多种功能,从维持组织内稳态(包括清除衰老红细胞和细胞碎片)到调节炎症和免疫。它们在控制血液期疟疾方面的作用仍不清楚。在此,我们表明,在缺乏组织驻留的CD169(+)巨噬细胞的情况下,伯氏疟原虫ANKA株(PbA)感染会导致寄生虫滞留显著增加,进而导致血管阻塞和渗漏以及疟色素疟原虫血红素在组织中的沉积增加。这会导致广泛的组织损伤,最终引发多器官炎症。因此,CD169(+)巨噬细胞控制寄生虫负荷及其在不同组织中的滞留以及限制感染诱导的炎症的能力对于减轻疟原虫感染和发病机制至关重要。

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Tissue-Resident CD169(+) Macrophages Form a Crucial Front Line against Plasmodium Infection.组织驻留型CD169(+)巨噬细胞构成抵御疟原虫感染的关键防线。
Cell Rep. 2016 Aug 9;16(6):1749-1761. doi: 10.1016/j.celrep.2016.07.010. Epub 2016 Jul 28.
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