Hepatitis B Virus e Antigen Physically Associates With Receptor-Interacting Serine/Threonine Protein Kinase 2 and Regulates IL-6 Gene Expression

作者:Wu Shuang; Kanda Tatsuo*; Imazeki Fumio; Nakamoto Shingo; Tanaka Takeshi; Arai Makoto; Roger Thierry; Shirasawa Hiroshi; Nomura Fumio; Yokosuka Osamu
来源:Journal of Infectious Diseases, 2012, 206(3): 415-420.
DOI:10.1093/infdis/jis363

摘要

We previously reported that hepatitis B virus (HBV) e antigen (HBeAg) inhibits production of interleukin 6 by suppressing NF-kappa B activation. NF-kappa B is known to be activated through receptor-interacting serine/threonine protein kinase 2 (RIPK2), and we examined the mechanisms of interleukin 6 regulation by HBeAg. HBeAg inhibits RIPK2 expression and interacts with RIPK2, which may represent 2 mechanisms through which HBeAg blocks nucleotide-binding oligomerization domain-containing protein 1 ligand-induced NF-kappa B activation in HepG2 cells. Our findings identified novel molecular mechanisms whereby HBeAg modulates intracellular signaling pathways by targeting RIPK2, supporting the concept that HBeAg could impair both innate and adaptive immune responses to promote chronic HBV infection.

  • 出版日期2012-8-1