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Therefore, we analysed regulatory mechanisms of TLR<\/jats:styled-content>3\u2010induced immune responses in nonparenchymal liver cells (NPC<\/jats:styled-content>s). Effects of Interleukin\u201010 (IL<\/jats:styled-content>\u201010), transforming growth factor beta (TGF<\/jats:styled-content>\u2010\u03b2) and immunoregulatory miR<\/jats:styled-content>\u2010155 on poly I<\/jats:styled-content>:C<\/jats:styled-content>\u2010activated murine (C<\/jats:styled-content>57BL<\/jats:styled-content>\/6) K<\/jats:styled-content>upffer cells (KC<\/jats:styled-content>) and sinusoidal endothelial cells (LSEC<\/jats:styled-content>) were assessed in vitro<\/jats:italic>. NPC<\/jats:styled-content>s were assayed for inflammatory and antiviral cytokines and T<\/jats:styled-content>\u2010cell (B<\/jats:styled-content>alb\/c)\u2010activating factors. Gene expression of miR<\/jats:styled-content>\u2010155, IL<\/jats:styled-content>\u201010, TGF<\/jats:styled-content>\u2010\u03b2 and interferon sensitive genes (ISG<\/jats:styled-content>s) in biopsies of patients with HCV<\/jats:styled-content> was determined by qrt\u2010PCR<\/jats:styled-content>. TLR<\/jats:styled-content>3\u2010induced antiviral activity in murine NPC<\/jats:styled-content>s was potently suppressed by IL<\/jats:styled-content>\u201010 and TGF<\/jats:styled-content>\u2010\u03b2 which correlated with decreased TLR<\/jats:styled-content>3 expression and inhibition of NF<\/jats:styled-content>\u2010\u03baB<\/jats:styled-content> and IRF<\/jats:styled-content>\u20103 activation. T\u2010cell activation, induced by TLR<\/jats:styled-content>3\u2010activated NPC<\/jats:styled-content>s, was also suppressed by IL<\/jats:styled-content>\u201010 and TGF<\/jats:styled-content>\u2010\u03b2, which was associated with a down\u2010regulation of CD<\/jats:styled-content>80 and CD<\/jats:styled-content>86. Pretreatment with IL<\/jats:styled-content>\u201010 or TGF<\/jats:styled-content>\u2010\u03b2 suppressed TLR<\/jats:styled-content>3\u2010induced miR<\/jats:styled-content>\u2010155 expression, which itself positively regulated poly I<\/jats:styled-content>:C<\/jats:styled-content>\u2010mediated immune responses, thus counteracting IL<\/jats:styled-content>\u201010 or TGF<\/jats:styled-content>\u2010\u03b2\u2010induced immunosuppression. In addition, hepatic expression of miR<\/jats:styled-content>\u2010155 was elevated in chronically infected patients with HCV<\/jats:styled-content>, was associated with an IL<\/jats:styled-content>\u201028B SNP<\/jats:styled-content> (rs12979860) and was inversely correlated with HCV<\/jats:styled-content> serum load and ISG<\/jats:styled-content> expression levels. As miR<\/jats:styled-content>\u2010155 is a key regulator of anti\u2010inflammatory mechanisms that control innate and adaptive hepatic immune responses during HCV<\/jats:styled-content> infection, miR<\/jats:styled-content>\u2010155 based therapies may represent a novel mechanism to control HCV<\/jats:styled-content> in the future.<\/jats:p>","DOI":"10.1111\/jvh.12126","type":"journal-article","created":{"date-parts":[[2013,9,12]],"date-time":"2013-09-12T01:12:54Z","timestamp":1378948374000},"page":"99-110","source":"Crossref","is-referenced-by-count":41,"title":["MicroRNA<\/scp>\u2010155 controls T<\/scp>oll\u2010like receptor 3\u2010 and hepatitis C<\/scp> virus\u2010induced immune responses in the liver"],"prefix":"10.1111","volume":"21","author":[{"given":"M.","family":"Jiang","sequence":"first","affiliation":[{"name":"Faculty of Medicine Department of Gastroenterology and Hepatology University Duisburg\u2010Essen Essen Germany"},{"name":"Faculty of Medicine Institute of Virology University Duisburg\u2010Essen Essen Germany"},{"name":"Department of Infectious Disease Union Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R.","family":"Broering","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Department of Gastroenterology and Hepatology University Duisburg\u2010Essen Essen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Trippler","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Department of Gastroenterology and Hepatology University Duisburg\u2010Essen Essen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Infectious Disease Union Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E.","family":"Zhang","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Institute of Virology University Duisburg\u2010Essen Essen Germany"},{"name":"Department of Infectious Disease Union Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"X.","family":"Zhang","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Institute of Virology University Duisburg\u2010Essen Essen Germany"},{"name":"Department of Infectious Disease Union Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G.","family":"Gerken","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Department of Gastroenterology and Hepatology University Duisburg\u2010Essen Essen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Lu","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Institute of Virology University Duisburg\u2010Essen Essen Germany"},{"name":"Department of Infectious Disease Union Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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