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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
Author(s) -
Zhang Jingshu,
Sze Daniel ManYuen,
Yung Benjamin YatMing,
Tang Petrus,
Chen WeiJune,
Chan KwokHung,
Leung Polly HangMei
Publication year - 2016
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12615
Subject(s) - dengue virus , biology , permissiveness , tetratricopeptide , virology , interferon , dengue fever , dendritic cell , innate immune system , immune system , virus , gene , immunology , viral replication , genetics
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.