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白细胞介素-18诱导小鼠自然杀伤细胞上高亲和力白细胞介素-2受体的表达，对于小鼠约氏疟原虫感染期间自然杀伤细胞产生γ干扰素至关重要。

IL-18-induced expression of high-affinity IL-2R on murine NK cells is essential for NK-cell IFN-γ production during murine Plasmodium yoelii infection.

作者信息

Stegmann Kerstin A, De Souza J Brian, Riley Eleanor M

机构信息

Faculty of Infectious and Tropical Diseases, Department of Immunology and Infection, London School of Hygiene and Tropical Medicine, London, UK.

Division of Infection and Immunity, University College London, London, UK.

出版信息

Eur J Immunol. 2015 Dec;45(12):3431-40. doi: 10.1002/eji.201546018. Epub 2015 Oct 21.

DOI:10.1002/eji.201546018
PMID:26420375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4982096/
Abstract

Early production of pro-inflammatory cytokines, including IFN-γ, is essential for control of blood-stage malaria infections. We have shown that IFN-γ production can be induced among human natural killer (NK) cells by coculture with Plasmodium falciparum infected erythrocytes, but the importance of this response is unclear. To further explore the role of NK cells during malaria infection, we have characterized the NK-cell response of C57BL/6 mice during lethal (PyYM) or nonlethal (Py17XNL) P. yoelii infection. Ex vivo flow cytometry revealed that NK cells are activated within 24 h of Py17XNL blood-stage infection, expressing CD25 and producing IFN-γ; this response was blunted and delayed during PyYM infection. CD25 expression and IFN-γ production were highly correlated, suggesting a causal relationship between the two responses. Subsequent in vitro experiments revealed that IL-18 signaling is essential for induction of CD25 and synergizes with IL-12 to enhance CD25 expression on splenic NK cells. In accordance with this, Py17XNL-infected erythrocytes induced NK-cell CD25 expression and IFN-γ production in a manner that is completely IL-18- and partially IL-12-dependent, and IFN-γ production is enhanced by IL-2. These data suggest that IL-2 signaling via CD25 amplifies IL-18- and IL-12-mediated NK-cell activation during malaria infection.

摘要

包括干扰素-γ在内的促炎细胞因子的早期产生对于控制血液期疟疾感染至关重要。我们已经表明，通过与恶性疟原虫感染的红细胞共培养，可在人类自然杀伤（NK）细胞中诱导干扰素-γ的产生，但这种反应的重要性尚不清楚。为了进一步探索NK细胞在疟疾感染期间的作用，我们对约氏疟原虫致死性（PyYM）或非致死性（Py17XNL）感染期间C57BL/6小鼠的NK细胞反应进行了表征。体外流式细胞术显示，在Py17XNL血液期感染的24小时内NK细胞被激活，表达CD25并产生干扰素-γ；在PyYM感染期间，这种反应减弱且延迟。CD25表达和干扰素-γ产生高度相关，表明这两种反应之间存在因果关系。随后的体外实验表明，IL-18信号传导对于CD25的诱导至关重要，并与IL-12协同作用以增强脾脏NK细胞上的CD25表达。与此一致，Py17XNL感染的红细胞以完全依赖IL-18和部分依赖IL-12的方式诱导NK细胞CD25表达和干扰素-γ产生，并且IL-2可增强干扰素-γ的产生。这些数据表明，在疟疾感染期间，通过CD25的IL-2信号传导放大了IL-18和IL-12介导的NK细胞激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/187f/4982096/40c7d3e53818/EJI-45-3431-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/187f/4982096/ee8caf802dbe/EJI-45-3431-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/187f/4982096/f88e9e54c03d/EJI-45-3431-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/187f/4982096/99424bd0e971/EJI-45-3431-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/187f/4982096/c4dcd58129fd/EJI-45-3431-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/187f/4982096/40c7d3e53818/EJI-45-3431-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/187f/4982096/ee8caf802dbe/EJI-45-3431-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/187f/4982096/f88e9e54c03d/EJI-45-3431-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/187f/4982096/99424bd0e971/EJI-45-3431-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/187f/4982096/c4dcd58129fd/EJI-45-3431-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/187f/4982096/40c7d3e53818/EJI-45-3431-g005.jpg

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