Vaccination with a DNA vaccine encoding CD317-targeting HBs antigen elicits enhanced immunity in mice
Conventional hepatitis B virus (HBV) vaccines fail to induce protective antibody titers in 5–10% of immune-competent vaccines. Therefore, safe and effective HBV vaccines are still clinically needed. In this study, we developed a plasmid DNA vaccine encoding CD317 single-chain fragment variable (α317...
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Veröffentlicht in: | Biochemical and biophysical research communications 2018-10, Vol.504 (4), p.865-870 |
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Sprache: | eng |
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Zusammenfassung: | Conventional hepatitis B virus (HBV) vaccines fail to induce protective antibody titers in 5–10% of immune-competent vaccines. Therefore, safe and effective HBV vaccines are still clinically needed.
In this study, we developed a plasmid DNA vaccine encoding CD317 single-chain fragment variable (α317scFv) linked with the hepatitis B surface antigen (HBsAg) and detected the humoral and cellular immune responses elicited by this vaccine in BALB/c mice.
Vaccination with this fusion DNA vaccine in BALB/c mice induced more robust antiviral T cell and antibody immunity against HBsAg. Compared with mice vaccinated with control vaccine encoding HBsAg, the level of serum-circulating anti-HBsAg antibody (HBsAb) was nearly double in fusion DNA-vaccinated mice. More interesting, splenic lymphocytes isolated from fusion DNA-vaccinated mice showed more potent proliferation and IFN-γ production after being re-stimulated with recombinant HBsAg in vitro. And not only that, the cytotoxicity of fusion DNA vaccine-sensitized splenocytes was ∼3-fold higher than that of controls.
Taken together, our results reveal that the fusion DNA vaccine can induce more effective immunological protection against HBV, and is a promising candidate for preventing HBV infection.
•DNA vaccine encoding CD317-targeting HBsAg induces more potent humoral immunity.•DNA vaccine encoding CD317-targeting HBsAg elicits more robust T cell response.•DNA vaccine encoding CD317-targeting HBsAg is a promising candidate for preventing HBV infection. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2018.09.024 |