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MiR-221 negatively regulates innate anti-viral response.
- Source :
-
PloS one [PLoS One] 2018 Aug 08; Vol. 13 (8), pp. e0200385. Date of Electronic Publication: 2018 Aug 08 (Print Publication: 2018). - Publication Year :
- 2018
-
Abstract
- The innate immune system plays a critical role in the initial antiviral response. However, the timing and duration of these responses must be tightly regulated during infection to ensure appropriate immune cell activation and anti-viral defenses. Here we demonstrate that during antiviral response, a negative regulator miR-221 was also induced in an ELF4-dependent manner. We further show that ELF4 promotes miR-221 expression through direct binding to its promoter. Overexpression and knockdown assay show that miR-221 can negatively regulate IFNβ production in time of virus infection. RNA-seq analysis of miR-221 overexpressed cells revealed multiple candidate targets. Taken together, our study identified a novel negative microRNA regulator of innate antiviral response, which is dependent on ELF4.<br />Competing Interests: The authors have declared that no competing interests exist.
- Subjects :
- Animals
Antagomirs metabolism
DNA-Binding Proteins deficiency
DNA-Binding Proteins genetics
Down-Regulation
HEK293 Cells
Herpesvirus 1, Human physiology
Humans
Interferon-beta genetics
Interferon-beta metabolism
Macrophages immunology
Macrophages metabolism
Macrophages virology
Mice
Mice, Inbred C57BL
Mice, Knockout
MicroRNAs antagonists & inhibitors
MicroRNAs genetics
Promoter Regions, Genetic
Protein Serine-Threonine Kinases genetics
Rhabdoviridae Infections pathology
Rhabdoviridae Infections virology
Transcription Factors deficiency
Transcription Factors genetics
Vesiculovirus genetics
Vesiculovirus immunology
Immunity, Innate genetics
MicroRNAs metabolism
Rhabdoviridae Infections immunology
Subjects
Details
- Language :
- English
- ISSN :
- 1932-6203
- Volume :
- 13
- Issue :
- 8
- Database :
- MEDLINE
- Journal :
- PloS one
- Publication Type :
- Academic Journal
- Accession number :
- 30089112
- Full Text :
- https://doi.org/10.1371/journal.pone.0200385