Mass Cytometric Analysis of HIV Entry, Replication, and Remodeling in Tissue CD4+ T Cells.
Mass Cytometric Analysis of HIV Entry, Replication, and Remodeling in Tissue CD4+ T Cells.
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DOI：
10.1016/j.celrep.2017.06.087
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发表时间：
2017-07-25
期刊：
影响因子：
8.8
通讯作者：
Roan NR
中科院分区：
文献类型：
--
作者：
Cavrois M;Banerjee T;Mukherjee G;Raman N;Hussien R;Rodriguez BA;Vasquez J;Spitzer MH;Lazarus NH;Jones JJ;Ochsenbauer C;McCune JM;Butcher EC;Arvin AM;Sen N;Greene WC;Roan NR
为了表征对HIV感染的易感性，我们通过单细胞质量细胞计数法对感染的扁桃体T细胞进行表型分析，并创建了全面的图谱，以确定哪些CD 4 + T细胞亚群支持HIV融合和生产性感染。通过降维、聚类和统计方法比较HIV融合细胞和HIV感染细胞以解释病毒扰动，我们确定了一个支持HIV进入但不支持病毒基因表达的记忆性CD 4 + T细胞亚群。这些细胞表达高水平的CD 127，IL-7受体，被认为是长寿的淋巴细胞。在HIV感染患者中，表达CD 127的细胞优先定位于滤泡外淋巴区域，病毒复制有限。因此，基于CyTOF的表型分析结合分析方法来区分病毒的选择性感染和受体调节可以用作发现工具。Cavrois等人通过CyTOF对HIV进入和组织CD 4 + T细胞的生产性感染进行了全面表征，并开发了一种分析方法，该方法利用CyTOF数据集的高维性质来区分感染期间调节的受体与优先感染细胞上差异表达的受体。
To characterize susceptibility to HIV infection, we phenotyped infected tonsillar T cells by single-cell mass cytometry and created comprehensive maps to identify which subsets of CD4+ T cells support HIV fusion and productive infection. By comparing HIV-fused and HIV-infected cells through dimensionality reduction, clustering, and statistical approaches to account for viral perturbations, we identified a subset of memory CD4+ T cells that support HIV entry but not viral gene expression. These cells express high levels of CD127, the IL-7 receptor, and are believed to be long-lived lymphocytes. In HIV-infected patients, CD127-expressing cells preferentially localize to extrafollicular lymphoid regions with limited viral replication. Thus, CyTOF-based phenotyping combined with analytical approaches to distinguish between selective infection and receptor modulation by viruses can be used as a discovery tool. Cavrois et al. conduct a global characterization of HIV entry and productive infection of tissue CD4+ T cells by CyTOF, and develop an analytical approach that takes advantage of the high-dimensional nature of CyTOF datasets to distinguish receptors modulated during infection from those differentially expressed on preferentially infected cells.
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影响因子：
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作者：
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通讯作者：
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DOI：
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影响因子：
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