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Distinct expression of interferon‐induced protein with tetratricopeptide repeats (IFIT) 1/2/3 and other antiviral genes between subsets of dendritic cells induced by dengue virus 2 infection

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]
卷期号:148 (4): 363-376 被引量:14
标识
DOI:10.1111/imm.12615
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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