A novel subset of putative stem/progenitor CD34+Oct-4+ cells is the major target for SARS coronavirus in human lung

被引:39
作者
Chen, Yongxiong
Chan, Vera Sau-Fong
Zheng, Bojian
Chan, Kelvin Yuen-Kwong
Xu, Xiaoning
To, Leo Yuk-Fai
Huang, Fang-Ping
Khoo, Ui-Soon
Lin, Chen-Lung Steve [1 ]
机构
[1] Univ Hong Kong, Dept Surg, Hong Kong, Hong Kong, Peoples R China
[2] Univ Hong Kong, Dept Microbiol, Hong Kong, Hong Kong, Peoples R China
[3] Univ Hong Kong, Li Ka Shing Fac Med, Dept Pathol, Hong Kong, Hong Kong, Peoples R China
[4] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Fac Med, Div Surg Oncol Reprod Biol & Anaesthet, London W12 0NN, England
[5] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Div Med, Dept Mol Genet & Rheumatol, London W12 0NN, England
[6] Univ Oxford, Weather Inst Mol Med, Human Immunol Unit, Oxford OX3 9DS, England
基金
英国医学研究理事会;
关键词
D O I
10.1084/jem.20070462
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Identification of the nature of severe acute respiratory syndrome (SARS)-infected cells is crucial toward understanding the pathogenesis. Using multicolor colocalization techniques, we previously reported that SARS(+) cells in the lung of fatally infected patients expressed the only known functional receptor, angiotensin-converting enzyme 2, and also a binding receptor, liver/lymph node-specific ICAM-3-grabbing non-integrin (CD209L). In this study, we show that SARS-infected cells also express the stem/progenitor cell markers CD34 and Oct-4, and do not express cytokeratin or surfactant. These putative lung stem/progenitor cells can also be identified in some non-SARS individuals and can be infected by SARS-coronavirus ex vivo. Infection of these cells may contribute to the loss of lung repair capacity that leads to respiratory failure as clinically observed.
引用
收藏
页码:2529 / 2536
页数:8
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