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Interferon Regulation Factor‐3 is a Critical Regulator of the Mature of Dendritic Cells from Mice
Author(s) -
Zhang G.,
Zhang Z.,
Liu Z.
Publication year - 2013
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12005
Subject(s) - interferon regulatory factors , gene knockdown , interferon , regulator , biology , microbiology and biotechnology , small interfering rna , irf1 , immune system , downregulation and upregulation , transfection , apoptosis , immunology , transcription factor , cell culture , gene , innate immune system , genetics
Interferon regulatory factor‐3 ( IRF ‐3) plays an important role in virus and double‐stranded RNA ‐mediated induction of type I interferon and RANTES (regulated on activation normal T cell expressed and secreted), DNA damage signalling, tumour suppression and virus‐induced apoptosis. IRF ‐3 had recently been shown to contribute to T ‐cell activation in response to pathogens, which implicated an extensive immunological role for IRF ‐3. Dendritic cells ( DC s) played critical roles as professional APC s in the development of immune responses. However, it was unclear whether IRF ‐3 had any effect on phenotype or function of DC s. In this study, it was shown that IRF ‐3 acted as a promoter of DC maturation. The level of IRF ‐3 expression was transiently upregulated and accumulated in the nucleus in TNF ‐α‐induced immune maturation of mice DC cells. Knockdown of IRF ‐3 by small interfering RNA in DC cells resulted in both phenotypic and functional immaturation, even without TNF ‐α treatment. Overall, our data demonstrated for the first time that IRF ‐3 was a critical regulator of mice DC maturation.