{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T13:24:16Z","timestamp":1791465856859,"version":"4.3.4"},"reference-count":54,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2018,10,1]],"date-time":"2018-10-01T00:00:00Z","timestamp":1538352000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,10,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>IFN-\u03bb is a cytokine expressed in epithelial tissues and plays a central role in antiviral mucosal immune response. The expression of IFN-\u03bb in the airway is impaired in chronic airway diseases (e.g., asthma, chronic obstructive pulmonary disease), which renders patients susceptible to viral infection. IL-17A is associated with asthma and chronic obstructive pulmonary disease pathogenesis; however, IL-17A regulation of IFN-\u03bb expression remains unclear. The aim of the current study is to clarify IL-17A\u2013mediated regulatory mechanisms of IFN-\u03bb expression in human airway epithelial cells. In this study, we have shown that polyinosinic:polycytidylic acid (polyI:C) and influenza A virus (IAV) infection increased IFN-\u03bb expression at mRNA and protein levels in primary cultures of normal human bronchial epithelial cells, whereas IL-17A attenuated polyI:C- or IAV-induced IFN-\u03bb expression. IFN-\u03bb receptor 1 knockdown and a JAK inhibitor, ruxolitinib, attenuated polyI:C-induced IFN-\u03bb expression, confirming that a positive autocrine feedback loop, the IFN-\u03bb receptor\u2013JAK\u2013STAT pathway, was involved in IFN-\u03bb expression. In Western blotting analysis, we demonstrated that polyI:C and IAV infection induced STAT1 phosphorylation in normal human bronchial epithelial cells, whereas IL-17A suppressed polyI:C- or IAV-mediated STAT1 phosphorylation. Furthermore, we found that cotreatment with IL-17A and polyI:C or IAV infection synergistically increased suppressor of cytokine signaling (SOCS)1 and SOCS3 expression. SOCS1 small interfering RNA and SOCS3 small interfering RNA negated the inhibitory effect of IL-17A in polyI:C-induced IFN-\u03bb expression by restoring attenuated STAT1 phosphorylation. Taken together, these findings indicate that IL-17A attenuates virus-induced IFN-\u03bb expression by enhancing SOCS1 and SOCS3 expression to inhibit autocrine signaling loops in human airway epithelial cells.<\/jats:p>","DOI":"10.4049\/jimmunol.1800147","type":"journal-article","created":{"date-parts":[[2018,9,17]],"date-time":"2018-09-17T10:45:20Z","timestamp":1537181120000},"page":"2392-2402","source":"Crossref","is-referenced-by-count":32,"title":["IL-17A Attenuates IFN-\u03bb Expression by Inducing Suppressor of Cytokine Signaling Expression in Airway Epithelium"],"prefix":"10.1093","volume":"201","author":[{"given":"Mitsuru","family":"Niwa","sequence":"first","affiliation":[{"name":"Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine , Hamamatsu, Shizuoka 431-3192 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