Identification of hepatitis C virus core domain inducing suppression of allostimulatory capacity of dendritic cells
Archives of Pharmacal Research, ISSN: 0253-6269, Vol: 25, Issue: 3, Page: 364-369
2002
- 12Citations
- 1Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations12
- Citation Indexes12
- 12
- CrossRef8
- Captures1
- Readers1
Article Description
Hepatitis C virus (HCV) is remarkably efficient at establishing chronic infection. One of the reasons for this appears to be the suppression of the accessory cell function of professional antigen presenting cells. In the present study, the immunosuppressive activity of HCV protein was examined on dendritic cells (DCs) generated from mouse bone marrow progenitor cells in vitro. We found that the DCs forced to express HCV protein have defective allostimulatory ability. DCs expressing HCV protein were phenotypically indistinguishable from normal DCs. However, they were unable to produce IL-12 effectively when stimulated with lipopolysaccharide. The functional domain of the HCV protein essential for immunosuppression was determined using a series of NH -and C-terminal deletion mutants of HCV core protein. We found that amino acid residues residing between the 21st and the 40th residues from the NH-terminus of HCV core protein are required for immunosuppression. These findings suggest that HCV core protein suppresses the elicitation of protective Th1 responses by the inhibition of IL-12 production by DCs.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0036599609&origin=inward; http://dx.doi.org/10.1007/bf02976640; http://www.ncbi.nlm.nih.gov/pubmed/12135111; https://link.springer.com/10.1007/BF02976640; https://dx.doi.org/10.1007/bf02976640; https://link.springer.com/article/10.1007/BF02976640; http://www.springerlink.com/index/10.1007/BF02976640; http://www.springerlink.com/index/pdf/10.1007/BF02976640
Springer Science and Business Media LLC
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