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This defect appears to be remedied by treatment with interferon\u2010\u03b1<\/jats:italic> (IFN<\/jats:styled-content>\u2010\u03b1<\/jats:italic>) \u2010based antiviral therapies; however, the molecular mechanisms underlying mDC<\/jats:styled-content> dysfunction in HCV<\/jats:styled-content> infection and restoration by IFN<\/jats:styled-content>\u2010\u03b1<\/jats:italic> treatment are unclear. The ubiquitin\u2010editing protein A20 plays a crucial role in controlling the maturation, cytokine production and immunostimulatory function of mDC<\/jats:styled-content>s. We propose that the expression of A20 correlates with the function of mDC<\/jats:styled-content>s during HCV<\/jats:styled-content> infection and IFN<\/jats:styled-content>\u2010\u03b1<\/jats:italic> therapy. In this study, we observed that A20 expression in mDC<\/jats:styled-content>s isolated from chronically HCV<\/jats:styled-content>\u2010infected subjects was significantly higher than healthy subjects or subjects achieving sustained virological responses (SVR<\/jats:styled-content>) following antiviral treatment. Notably, A20 expression in mDC<\/jats:styled-content>s from HCV<\/jats:styled-content> patients during IFN<\/jats:styled-content>\u2010\u03b1<\/jats:italic> treatment was significantly lower than for untreated patients, SVR<\/jats:styled-content> patients, or healthy subjects. Besides, A20 expression in mDC<\/jats:styled-content>s stimulated by polyI:C differed between HCV<\/jats:styled-content> patients and healthy subjects, and this difference could be abrogated by the treatment with IFN<\/jats:styled-content>\u2010\u03b1 in vitro<\/jats:italic>. Additionally, A20 expression by polyI:C\u2010activated mDC<\/jats:styled-content>s, with or without IFN<\/jats:styled-content>\u2010\u03b1<\/jats:italic> treatment, negatively correlated with the expression of HLA<\/jats:styled-content>\u2010DR<\/jats:styled-content>, CD<\/jats:styled-content>86 and CC<\/jats:styled-content>R7, and the secretion of interleukin\u201012 (IL<\/jats:styled-content>\u201012), but positively associated with the production of IL<\/jats:styled-content>\u201010. Importantly, silencing A20 expression using small interfering RNA<\/jats:styled-content>s increased the production of IL<\/jats:styled-content>\u201012 in mDC<\/jats:styled-content>s of chronically HCV<\/jats:styled-content>\u2010infected individuals. These findings suggest that A20 plays a crucial role in negative regulation of innate immune responses during chronic viral infection.<\/jats:p>","DOI":"10.1111\/imm.12350","type":"journal-article","created":{"date-parts":[[2014,6,25]],"date-time":"2014-06-25T16:52:03Z","timestamp":1403715123000},"page":"670-678","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Role of A20 in interferon\u2010\u03b1<\/i>\u2010mediated functional restoration of myeloid dendritic cells in patients with chronic hepatitis C"],"prefix":"10.1111","volume":"143","author":[{"given":"Li","family":"Ma","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases Tangdu Hospital The Fourth Military Medical University Xi'an China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yun","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases Tangdu Hospital The Fourth 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