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Hepatitis B virus (HBV) is a noncytopathic DNA virus and is the pathogen of acute and chronic hepatitis. Interferon and nucleotide analogues such as lamivudine and adefovir are the current treatment strategies of HBV infection; however, it is still a serious disease. Therefore, the development of new therapeutic options against HBV is needed. In the present study, we have investigated whether the vectors carrying short hairpin RNA (shRNA) targeting the murine B7-DC gene could silence the expression of B7-DC and analyzed the function of gene-modified dendritic cells (DCs) by mixed lymphocyte reaction. The results demonstrated that two shRNA vectors efficiently suppressed the expression of B7-DC. The MLR assay showed that shRNA-B7-DC-transfected DCs induced markedly higher allogeneic lymphocyte proliferation than transfected DCs with the vector plasmid pAS and untreated DCs at all dilutions. The most efficient shRNA plasmid vector against B7-DC was then used to silence the expression of B7-DC on DCs, the gene-modified DCs were pulsed with HBV-specific peptides, and HBV transgenic mice were immunized. After three rounds of immunization, the splenocytes were stimulated in vitro and tested for cytotoxicitic T lymphocyte activity, while the sera were used to detect the level of HBsAg and HBV DNA. The data demonstrated that blockade of B7-DC on DCs augmented the cytolytic activity induced by immunization with peptide-pulsed DCs and significantly reduced the concentration of serum HBsAg and HBV DNA, suggesting that silencing of B7-DC is of potential value in DC-based therapy of HBV infection.
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Article Synopsis
- The B7 family molecules play a role in immune responses and cancer, but their specific expression and impact on acute myeloid leukemia (AML) is not well understood, necessitating research through bioinformatics databases.
- The study analyzed B7 molecule expression and their prognostic significance in AML using various databases, revealing that high expression of certain B7 members is linked to poor patient outcomes, while others may have protective effects.
- Findings indicate that genetic alterations and co-expression patterns of B7 family members may contribute to AML development and prognosis, suggesting their potential as biomarkers and therapeutic targets.
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