登革热病毒
生物
宽容
四三肽
病毒学
干扰素
登革热
树突状细胞
先天免疫系统
免疫系统
病毒
基因
免疫学
病毒复制
遗传学
作者
Jing Shu Zhang,Daniel Sze,Benjamin Yat‐Ming Yung,Petrus Tang,Wei‐June Chen,Kwok‐Hung Chan,Polly H. M. Leung
出处
期刊:Immunology
[Wiley]
日期:2016-05-02
卷期号:148 (4): 363-376
被引量:14
摘要
Summary Dengue virus ( DENV ) infection is an emerging public health hazard threatening inhabitants of the tropics and sub‐tropics. Dendritic cells ( DC s) are one of the major targets of DENV and the initiators of the innate immune response against the virus. However, current in vitro research on the DENV – DC interaction is hampered by the low availability of ex vivo DC s and donor variation. In the current study, we attempted to develop a novel in vitro DC model using immature DCs derived from the myeloid leukaemia cell line MUTZ ‐3 ( IMDC s) to investigate the DENV – DC interaction. The IMDC s morphologically and phenotypically resembled human immature monocyte‐derived dendritic cells ( IMM o DC s). However, the permissiveness of IMDC s to DENV 2 was lower than that of IMM o DC s. RT ‐ PCR arrays showed that a group of type I interferon ( IFN ) ‐inducible genes, especially IFIT 1, IFITM 1, and IFI 27, were significantly up‐regulated in IMM o DC s but not in IMDC s after DENV 2 infection. Further investigation revealed that IFIT genes were spontaneously expressed at both transcriptional and protein levels in the naive IMDC s but not in the naive IMM o DC s. It is possible that the poor permissiveness of IMDC s to DENV 2 was a result of the high basal levels of IFIT proteins. We conclude that the IMDC model, although less permissive to DENV 2, is a useful platform for studying the suppression mechanism of DENV 2 and we expand the knowledge of cellular factors that modulate DENV 2 infection in the human body.
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