Non-random lymphocyte distribution among virus-infected cells of the respiratory tract.

Non-random lymphocyte distribution among virus-infected cells of the respiratory tract.
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呼吸道病毒感染细胞中淋巴细胞的非随机分布。

DOI:
10.1089/vim.2013.0033
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发表时间:
2013
期刊:
影响因子:
2.2
通讯作者:
Hurwitz,JuliaL
Hurwitz,JuliaL
中科院分区:
医学4区
文献类型:
--
作者:
Rudraraju,Rajeev;Sealy,RobertE;Surman,SherriL;Thomas,PaulG;Dayton,BarryH;Hurwitz,JuliaL

文献摘要

相似文献

T细胞在病毒感染的呼吸道组织中的定位规则知之甚少。因此,我们标记了仙台病毒(SeV)致敏小鼠的颈部淋巴结或脾细胞,并将淋巴细胞转移到表达增强型绿色荧光蛋白(SeV-eGFP)的SeV感染的动物中。共聚焦成像显示,当T细胞进入受感染的呼吸道上皮时,它们呈现出一种空间分布,使每个供体细胞与其最近邻细胞之间的距离最大化。因此,我们假设淋巴细胞通过改变它们的趋化因子/细胞因子微环境来相互排斥。随后的体外试验证实,当SeV引发的淋巴细胞与感染的呼吸道基质共培养时,趋化因子包括RANTES、CXCL 9、CXCL 10和CCL 2显著上调。基于这些数据,我们提出,病毒感染的呼吸道组织内新驻留的淋巴细胞可能会产生趋化因子/细胞因子的晕圈来标记它们的领土;淋巴细胞的串扰可能会抑制细胞重叠和冗余,以加快病毒清除。
The rules of T cell positioning within virus-infected respiratory tract tissues are poorly understood. We therefore marked cervical lymph node or spleen cells from Sendai virus (SeV) primed mice and transferred lymphocytes to animals infected with SeV expressing an enhanced green fluorescent protein (SeV-eGFP). Confocal imaging showed that when T cells entered a field of infected respiratory tract epithelium, they assumed a spatial distribution that maximized distances between each donor cell and its nearest neighbor. We therefore hypothesized that lymphocytes repelled one another by altering their chemokine/cytokine microenvironment. Subsequentin vitrotests confirmed that when SeV-primed lymphocytes were co-cultured with infected respiratory tract stroma, there was a profound upregulation of chemokines including RANTES, CXCL9, CXCL10, and CCL2. Based on these data, we propose that newly resident lymphocytes within virus-infected respiratory tract tissues may create halos of chemokines/cytokines to mark their territories; lymphocyte cross-talk may then inhibit cell overlap and redundancy to expedite virus clearance.