Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 206, Issue 3, Pages 415-420Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jis363
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Funding
- Japan Science and Technology Agency, Ministry of Education, Culture, Sports, Science, and Technology, Japan [21590829, 21590828]
- Japan Society of Hepatology
- Chiba University Young Research-Oriented Faculty Member Development Program in Bioscience Areas
- Miyakawa Memorial Research Foundation
- Grants-in-Aid for Scientific Research [21590829, 21590828] Funding Source: KAKEN
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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.
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