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Genetic vaccination with Flt3-L and GM-CSF as adjuvants: Enhancement of cellular and humoral mmune responses that results in protective immunity in a murine model of hepatitis C virus infection

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World Journal of Gastroenterology 2006年第44期12卷 7118-7125页

作者： Jens Encke Jomo Bernardin Jasmin Geib Gocha Barbakadze raymond bujdoso Wolfgang Stremmel Department of InternalMedicine IV University of Heidelberg Im Neuenheimer Feld410 69120 Heidelberg Germany Department of Immunology University of Heidelberg Im Neuenheimer Feld 305 69120 Heidelberg Germany Department of InternalMedicine IV University of Heidelberg Im Neuenheimer Feld410 69120 Heidelberg Germany Department of Clinical Veterinary Medicine University of Cambridge Madingley Road Cambridge CB3 OES United Kingdom

AIM： To investigate whether transfection of plasmid DNA encoding these cytokines enhances both humoral and cellular immune responses to hepatitis C virus （HCV） in a murine model. METHODS： We established a tumor model of HCV infection using syngenic mouse myeloma cells stably transfected with NS5. Co-vaccination of DNA encoding granulocyte macrophage colony-stimulating factor （GM- CSF） and Flt-3 ligand together with a plasmid encoding for the HCV NS5 protein was carried out. Mice were sacrificed 14 d after the last immunization event with collection of spleen cells and serum to determine humoral and cellular immune responses. RESULTS： Co-vaccination of DNA encoding GM-CSF and Fit-3 ligand together with a plasmid encoding for the HCV NS5 protein induced increased antibody responses and CD4＋ T cell proliferation to this protein, Vaccination with DNA encoding GM-CSF and FIt-3L promoted protection against tumor formation and/or reduction in mice co- immunized with cytokine-encoding DNA constructs, This suggests this strategy is capable of generating cytotoxic T lymphocyte activity in vivo, Following inoculation with plasmid DNA encoding Flt-3L, no increase in spleen size or in dendritic cell （DC） and natural killer cell numbers was observed. This was in contrast to a dramatic increase of both cell types after administration of recombinant Flt3-L in vivo. This suggests that vaccination with plasmid DNA encoding cytokines that regulate DC generation and mobilization may not promote unwanted side effects, such as autoimmunity, splenic fibrosis or hematopoietic malignancies that may occur with administration of recombinant forms of these proteins. CONCLUSION： Our data support the view that plasmid DNA vaccination is a promising approach for HCV immunization, and may provide a general adjuvant vaccination strategy against malignancies and other pathogens.

关键词： DNA-vaccination Dendritic cells Flt3-L granulocyte macrophage colony-stimulating factor Hepatitis C virus

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Prion-induced neurotoxicity: Possible role for cell cycle activity and DNA damage response

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World Journal of Virology 2015年第3期4卷 188-197页

作者： raymond bujdoso Matthias Landgraf Walker S Jackson Alana M Thackray Department of Veterinary Medicine University of Cambridge Department of Zoology University of Cambridge German Center for Neurodegenerative Disease (DZNE)

Protein misfolding neurodegenerative diseases arisethrough neurotoxicity induced by aggregation of host proteins. These conditions include Alzheimer's disease, Huntington's disease, Parkinson's disease, motor neuron disease, tauopathies and prion diseases. Collectively, these conditions are a challenge to society because of the increasing aged population and through the real threat to human food security by animal prion diseases. It is therefore important to understand the cellular and molecular mechanisms that underlie protein misfolding--induced neurotoxicity as this will form the basis for designing strategies to alleviate their burden. Prion diseases are an important paradigm for neurodegenerative conditions in general since several of these maladies have now been shown to display prion--like phenomena. Increasingly, cell cycle activity and the DNA damage response are recognised as cellular events that participate in the neurotoxic process of various neurodegenerative diseases, and their associated animal models, which suggests they are truly involved in the pathogenic process and are not merely epiphenomena. Here we review the role of cell cycle activity and the DNA damage response in neurodegeneration associated with protein misfolding diseases, and suggest that these events contribute towards prion--induced neurotoxicity. In doing so, we highlight PrP transgenic Drosophila as a tractable model for the genetic analysis of transmissible mammalian prion disease.

关键词： Neurodegenerative disease Protein misfolding Prion Transmissible Cell cycle DNA repair Chromatin PrP transgenic Drosophila

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