IL-17A but not IL-22 suppresses the replication of hepatitis B virus mediated by over-expression of MxA and OAS mRNA in the HepG2.2.15 cell line

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• 作者：Bing Wang^a ; ^b ; Xin-Ping Zhao^c ; Yu-Chen Fan^a ; ^b ; Jian-Jun Zhang^a ; Jing Zhao^a ; Kai Wang^a ; ^b ; ^{wangdoc876@126.com} ; ^{wangdoc876@yahoo.com.cn}
• 关键词：HBV ; hepatitis B virus ; HBeAg ; hepatitis B e antigen ; HBsAg ; hepatitis B surface antigen ; TH17 ; T helper 17 ; IL-17A ; interleukin-17A ; IL-22 ; Interleukin-22 ; Ab ; antibody ; MxA ; myxovirus resistance A ; OAS ; oligoadenylate synthetase ; ISFG3 ; IFN-stimulated g
• 刊名：Antiviral Research
• 出版年：2013
• 出版时间：March, 2013
• 年：2013
• 卷：97
• 期：3
• 页码：285-292
• 全文大小：544 K

文摘

Interleukin-17A (IL-17A) and interleukin-22 (IL-22), mainly secreted by interleukin-17-producing T help cells (Th17), are pleiotropic cytokines that regulate the biological responses of several target cells, including hepatocytes. Th17 frequency was reported to negatively correlate with plasma hepatitis B virus (HBV) DNA load in patients with HBV infection. Several studies have indicated that cytokines, such as IL-6 and IL-4, are involved in the noncytopathic suppression of HBV replication. We therefore hypothesized that IL-17A and IL-22 might have a potent suppressive effect on HBV replication. In our present study, we analyzed the suppressive effect of IL-17A and IL-22 on HBV replication in the hepatocellular carcinoma cell line HepG2.2.15. IL-17A did not inhibit the proliferation of HepG2.2.15 cells. It decreased the levels of HBV s antigen (HBsAg) and HBV e antigen (HBeAg) in culture medium and the levels of intracellular HBV DNA. By contrast, blockage of IL-17 receptor (IL-17R) increased the levels of HBsAg and extracellular HBV DNA in culture medium and the levels of intracellular HBV DNA. The expression of antiviral proteins, including myxovirus resistance A (MxA) and oligoadenylate synthetase (OAS), was enhanced by IL-17A. IL-22 and anti-human IL-22 receptor (IL-22R) antibody did not change any indexes. We demonstrated that IL-17A effectively suppressed HBV replication in a noncytopathic manner and the over-expression of MxA and OAS mRNA was involved in the suppression of HBV replication by IL-17A.