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© Research
Publication : Frontiers in immunology

IFN-I inducible miR-3614-5p targets ADAR1 isoforms and fine tunes innate immune activation.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Frontiers in immunology - 01 Jan 2022

Vuillier F, Li Z, Black I, Cruciani M, Rubino E, Michel F, Pellegrini S,

Link to Pubmed [PMID] – 35935998

Link to DOI – 10.3389/fimmu.2022.939907

Front Immunol 2022 ; 13(): 939907

Regulation of innate immune responses is essential for maintenance of immune homeostasis and development of an appropriate immunity against microbial infection. We show here that miR-3614-5p, product of the TRIM25 host gene, is induced by type I interferon (IFN-I) in several human non-immune and immune cell types, in particular in primary myeloid cells. Studies in HeLa cells showed that miR-3614-5p represses both p110 and p150 ADAR1 and reduces constitutive and IFN-induced A-to-I RNA editing. In line with this, activation of innate sensors and expression of IFN-β and the pro-inflammatory IL-6 are promoted. MiR-3614-5p directly targets ADAR1 transcripts by binding to one specific site in the 3’UTR. Moreover, we could show that endogenous miR-3614-5p is associated with Ago2 and targets ADAR1 in IFN-stimulated cells. Overall, we propose that, by reducing ADAR1, IFN-I-induced miR-3614-5p contributes to lowering the activation threshold of innate sensors. Our findings provide new insights into the role of miR-3614-5p, placing it as a potential fine tuner of dsRNA metabolism, cell homeostasis and innate immunity.