Full metadata record
DC Field | Value | Language |
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dc.creator | Lasarte, J.J. (Juan José) | - |
dc.creator | Corrales, F.J. (Fernando José) | - |
dc.creator | Casares, N. (Noelia) | - |
dc.creator | Lopez-Diaz-de-Cerio, A. (Ascensión) | - |
dc.creator | Qian, C. (Cheng) | - |
dc.creator | Xie, X. (Xiaoming) | - |
dc.creator | Borras-Cuesta, F. (Francisco) | - |
dc.creator | Prieto, J. (Jesús) | - |
dc.date.accessioned | 2012-04-02T07:52:20Z | - |
dc.date.available | 2012-04-02T07:52:20Z | - |
dc.date.issued | 1999 | - |
dc.identifier.citation | Lasarte JJ, Corrales FJ, Casares N, Lopez-Diaz de Cerio A, Qian C, Xie X, et al. Different doses of adenoviral vector expressing IL-12 enhance or depress the immune response to a coadministered antigen: the role of nitric oxide. J Immunol 1999 May 1;162(9):5270-5277. | es_ES |
dc.identifier.issn | 1550-6606 | - |
dc.identifier.uri | https://hdl.handle.net/10171/21489 | - |
dc.description.abstract | Joint immunization with two recombinant adenoviruses, one expressing hepatitis C virus (HCV) core and E1 proteins and another expressing IL-12 (RAdIL-12), strongly potentiates cellular immune response against HCV Ags in BALB/c mice when RAdIL-12 was used at doses of 1 x 105-1 x 107 plaque-forming units. However, cellular immunity against HCV Ags was abolished when higher doses (1 x 108 plaque-forming units) of RAdIL-12 were used. This immunosuppressive effect was associated with marked elevation of IFN-gamma and nitric oxide in the serum and increased cell apoptosis in the spleen. Administration of N-nitro-L -arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, to mice that received high doses of RAdIL-12 was lethal, whereas no apparent systemic toxicity by L -NAME was observed in those immunized with lower doses of the adenovirus. Interestingly, in mice immunized with recombinant adenovirus expressing core and E1 proteins of HCV in combination with RAdIL-12 at low doses (1 x 107 plaque-forming units), L -NAME inhibited T cell proliferation and CTL activity in response to HCV Ags and also production of Abs against adenoviral proteins. In conclusion, gene transfer of IL-12 can increase or abolish cell immunity against an Ag depending of the dose of the vector expressing the cytokine. IL-12 stimulates the synthesis of NO which is needed for the immunostimulating effects of IL-12, but apoptosis of T cells and immunosuppression ensues when IFN-gamma and NO are generated at very high concentrations. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | American Association of Immunologists | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.subject | Adenoviridae/genetics | es_ES |
dc.subject | Adenoviridae/immunology | es_ES |
dc.subject | Antigens, Viral/immunology | es_ES |
dc.subject | Genetic Vectors/administration & dosage | es_ES |
dc.subject | Genetic Vectors/immunology | es_ES |
dc.subject | Interleukin-12/genetics | es_ES |
dc.subject | Nitric Oxide/physiology | es_ES |
dc.title | Different doses of adenoviral vector expressing IL-12 enhance or depress the immune response to a coadministered antigen: the role of nitric oxide | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.relation.publisherversion | http://jimmunol.org/content/162/9/5270 | es_ES |
dc.type.driver | info:eu-repo/semantics/article | es_ES |
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