| First Author | Meng Y | Year | 2020 |
| Journal | JCI Insight | Volume | 5 |
| Issue | 8 | PubMed ID | 32213710 |
| Mgi Jnum | J:341776 | Mgi Id | MGI:6717722 |
| Doi | 10.1172/jci.insight.133721 | Citation | Meng Y, et al. (2020) MicroRNA-148a facilitates inflammatory dendritic cell differentiation and autoimmunity by targeting MAFB. JCI Insight 5(8) |
| abstractText | Monocyte-derived DCs (moDCs) have been implicated in the pathogenesis of autoimmunity, but the molecular pathways determining the differentiation potential of these cells remain unclear. Here, we report that microRNA-148a (miR-148a) serves as a critical regulator for moDC differentiation. First, miR-148a deficiency impaired the moDC development in vitro and in vivo. A mechanism study showed that MAFB, a transcription factor that hampers moDC differentiation, was a direct target of miR-148a. In addition, a promoter study identified that miR-148a could be transcriptionally induced by PU.1, which is crucial for moDC generation. miR-148a ablation eliminated the inhibition of PU.1 on MAFB. Furthermore, we found that miR-148a increased in monocytes from patients with psoriasis, and miR-148a deficiency or intradermal injection of antagomir-148a immensely alleviated the development of psoriasis-like symptoms in a psoriasis-like mouse model. Therefore, these results identify a pivotal role for the PU.1-miR-148a-MAFB circuit in moDC differentiation and suggest a potential therapeutic avenue for autoimmunity. |
