MafB, a target of microRNA-155, regulates dendritic cell maturation

Author:

Yang Lu12,Li Rui12,Xiang Shaoxun3,Xiao Weihua12

Affiliation:

1. 2The CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China

2. 3Hefei National Laboratory for Physical Sciences at Microscale, Engineering Technology Research Center of Biotechnology Drugs, University of Science and Technology of China, Hefei, Anhui 230027, China

3. 1CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science & Technology of China

Abstract

AbstractMafB is a member of bZip transcription factors that share similar basic region/leucine zipper DNA binding motifs and N-terminal activation domains. It is well known that MafB is highly expressed in macrophages and promotes differentiation of myeloid progenitors into macrophage. However, little is known about its function in dendritic cells. Here, we report that MafB, as a target of miR-155, which had been reported to be required for dendritic cell maturation and function, regulated dendritic cell maturation. MafB and miR-155were reversely correlated during DC maturation induced by LPS and forced expression of miR-155 reduced MafB expression. The luciferase reporter assay showed that MafB 3’UTR was directly targeted bymiR-155. In addition, knockdown of MafB promoted the phenotypic maturation of DC2.4 cells. Forced expression of MafB could significantly attenuate the phenotypic maturation of DC2.4 cells caused by overexpression of miR-155. Overall, our data demonstrates that MafB, inhibited by miR-155, was a negative regulator of DC maturation.

Publisher

Walter de Gruyter GmbH

Subject

General Agricultural and Biological Sciences,General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Neuroscience

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