Hepatitis C virus (HCV) causes a persistent infection, chronic hepatitis, and leads to hepatocellular carcinoma. Nonstructural protein 3 (NS3) of HCV possesses protease, nucleoside triphosphatase, and helicase activities. Using the yeast two hybrid assay, we identified Sm-D1, a host protein that binds to NS3. Sm-D1 is a component of small nuclear ribonucleoprotein (snRNP) complexes which are associated with autoimmune disease. Sm-D1 has Gly-Arg (GR) repeats at the C terminus, which contains dimethylarginine modified by post-translational modification and may constitute an immunoreactive determinant. Deletion mutants revealed that the C-terminal region of Sm-D1 containing the GR repeats was the binding region for NS3, and the expression feature of Sm-D1 was affected by co-expression of NS3. Immunostaining assay demonstrated that NS3 was also present in the nucleus of cells overexpressing Sm-D1, although it was usually found in cytoplasm. The localization of NS3 could change following interaction with Sm-D1 and affect the function of Sm-D1.
References
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This 2002 study investigated the effect of β-1,3-glucan on monocyte immunostimulation, examining both direct and indirect pathways of immune cell activation in human blood.
β-1,3-glucan significantly stimulated monocyte production of pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6. The stimulation was dose-dependent and occurred through both direct receptor-mediated activation and complement-mediated pathways. These findings established monocytes as key responders to β-glucan immunostimulation.
Monocyte activation represents a key innate immune response to β-glucan supplementation. This research supports the mechanism by which orally administered Aureobasidium pullulans β-glucan can drive systemic immune activation through monocyte stimulation.
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Iwai, Atsushi; Hasumura, Yasushi; Nojima, Takayuki; Takegami, Tsutomu. Hepatitis C Virus Nonstructural Protein NS3 Binds to Sm-D1, a Small Nuclear Ribonucleoprotein Associated with Autoimmune Disease. Microbiology and Immunology. 2003. DOI: 10.1111/j.1348-0421.2003.tb03423.x.
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