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Título: | Association of MicroRNA-618 Expression With Altered Frequency and Activation of Plasmacytoid Dendritic Cells in Patients With Systemic Sclerosis |
Autor: | Rossato, M; Affandi, A.J.; Thordardottir, S; Wichers, CGK; Cossu, M.; Broen, Jasper C.; Moret, FM; Bossini-Castillo, L.; Chouri, E.; van Bon, L; Wolters, F; Marut, W.; van der Kroef, M; Silva-Cardoso, S; Bekker, C.P.J.; Dolstra, H; van Laar, JM; Martín, J.; van Roon, JAG; Reedquist, KA; Beretta, L.; Radstake, T. R. | Fecha de publicación: | sep-2017 | Editor: | John Wiley & Sons | Citación: | Arthritis and Rheumatology | Resumen: | Objective. Plasmacytoid dendritic cells (PDCs) are a critical source of type I interferons (IFNs) that can contribute to the onset and maintenance of autoimmunity. Molecular mechanisms leading to PDC dysregulation and a persistent type I IFN signature are largely unexplored, especially in patients with systemic sclerosis (SSc), a disease in which PDCs infiltrate fibrotic skin lesions and produce higher levels of IFN alpha than those in healthy controls. This study was undertaken to investigate potential microRNA (miRNA)-mediated epigenetic mechanisms underlying PDC dysregulation and type I IFN production in SSc. Methods. We performed miRNA expression profiling and validation in highly purified PDCs obtained from the peripheral blood of 3 independent cohorts of healthy controls and SSc patients. Possible functions of miRNA-618 (miR-618) on PDC biology were identified by overexpression in healthy PDCs. Results. Expression of miR-618 was up-regulated in PDCs from SSc patients, including those with early disease who did not present with skin fibrosis. IFN regulatory factor 8, a crucial transcription factor for PDC development and activation, was identified as a target of miR-618. Overexpression of miR-618 reduced the development of PDCs from CD34+ cells in vitro and enhanced their ability to secrete IFN alpha, mimicking the PDC phenotype observed in SSc patients. Conclusion. Up-regulation of miR-618 suppresses the development of PDCs and increases their ability to secrete IFN alpha, potentially contributing to the type I IFN signature observed in SSc patients. Considering the importance of PDCs in the pathogenesis of SSc and other diseases characterized by a type I IFN signature, miR-618 potentially represents an important epigenetic target to regulate immune system homeostasis in these conditions. | URI: | http://hdl.handle.net/10261/177354 | DOI: | 10.1002/art.40163 | ISSN: | 2326-5191 | E-ISSN: | 2326-5205 |
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