| Autor: |
Wu S; Department of Medicine and Clinical Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan., Kanda T, Imazeki F, Nakamoto S, Tanaka T, Arai M, Roger T, Shirasawa H, Nomura F, Yokosuka O |
| Jazyk: |
angličtina |
| Zdroj: |
The Journal of infectious diseases [J Infect Dis] 2012 Aug 01; Vol. 206 (3), pp. 415-20. Date of Electronic Publication: 2012 May 21. |
| DOI: |
10.1093/infdis/jis363 |
| Abstrakt: |
We previously reported that hepatitis B virus (HBV) e antigen (HBeAg) inhibits production of interleukin 6 by suppressing NF-κB activation. NF-κB 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-κB 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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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