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The expression of microRNA\u2010146a (miR\u2010146a) is reduced in the white blood cells of SLE patients and accounts for their overactivated inflammatory responses. However, the mechanism of the reduction of miR\u2010146a is still not fully understood. This study was undertaken to test whether the key pathogenic cytokine, type I IFN, is responsible for the dysregulation of miR\u2010146a in SLE.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Gene and protein expression was measured in all cells by reverse transcription\u2013quantitative polymerase chain reaction, Northern blotting, or Western blotting. In THP\u20101 cells, expression of monocyte chemotactic protein\u2013induced protein 1 (MCPIP\u20101) was knocked down with a lentivirus encoding a short hairpin RNA targeting <jats:italic>MCPIP1<\/jats:italic>. The cells were pretreated with type I IFN and assessed for gene expression levels of miR\u2010146a. White blood cells from patients with SLE were analyzed for the expression of the IFN\u2010inducible genes <jats:italic>MCPIP1<\/jats:italic> and miR\u2010146a, and the gene expression data were compared for correlation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Pretreatment of THP\u20101 cells with type I IFN attenuated the induction of miR\u2010146a posttranscriptionally, by down\u2010regulating the expression of pre\u2010miR\u2010146a but not pri\u2010miR\u2010146a or its original unspliced transcript. Expression of MCPIP\u20101, which was enhanced by type I IFN, was found to be responsible for the inhibition of miR\u2010146a. In white blood cells from patients with SLE, <jats:italic>MCPIP1<\/jats:italic> expression was elevated, and its expression correlated positively with the IFN score and negatively with the miR\u2010146a transcript level.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Type I IFN inhibits the maturation of miR\u2010146a through the up\u2010regulation of MCPIP\u20101, and thus contributes to the uncontrolled inflammation and excessive inflammatory gene expression in SLE.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.39398","type":"journal-article","created":{"date-parts":[[2015,8,28]],"date-time":"2015-08-28T11:50:35Z","timestamp":1440762635000},"page":"3209-3218","source":"Crossref","is-referenced-by-count":60,"title":["Type I Interferon Inhibition of MicroRNA\u2010146a Maturation Through Up\u2010Regulation of Monocyte Chemotactic Protein\u2013Induced Protein 1 in Systemic Lupus Erythematosus"],"prefix":"10.1002","volume":"67","author":[{"given":"Bo","family":"Qu","sequence":"first","affiliation":[{"name":"Renji Hospital, Shanghai Jiao Tong University School of Medicine, Institute of Health Sciences of Shanghai Institutes for Biological Sciences, and Chinese Academy of Sciences Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianchang","family":"Cao","sequence":"additional","affiliation":[{"name":"Institute of Health Sciences of Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feifei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Institute of Health Sciences of Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, and Shanghai Jiao Tong University School of Medicine Shanghai 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