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The subcellular location of antigen expressed by adenoviral vectors modifies adaptive immunity but not dependency on cross-presenting dendritic cells.

Artikel i vetenskaplig tidskrift
Författare Petra Henning
Tobias Gustafsson
Carl-Fredrik Flach
Yeu-Jiann Hua
Anna Strömbeck
Jan Holmgren
Leif Lindholm
Ulf Yrlid
Publicerad i European journal of immunology
Volym 41
Nummer/häfte 8
Sidor 2185-96
ISSN 1521-4141
Publiceringsår 2011
Publicerad vid Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Sidor 2185-96
Språk en
Länkar dx.doi.org/10.1002/eji.201041009
Ämnesord Adaptive Immunity, immunology, Adenoviridae, genetics, immunology, Animals, Antigens, genetics, immunology, metabolism, Cell Line, Cell Line, Tumor, Cross-Priming, immunology, Dendritic Cells, immunology, metabolism, Female, Flow Cytometry, Genetic Vectors, genetics, immunology, Green Fluorescent Proteins, genetics, immunology, metabolism, HEK293 Cells, Humans, Immunization, methods, Immunoglobulin A, immunology, metabolism, Immunoglobulin G, blood, immunology, Lung, immunology, metabolism, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Ovalbumin, genetics, immunology, metabolism, T-Lymphocytes, immunology, metabolism, T-Lymphocytes, Cytotoxic, immunology, metabolism, Transduction, Genetic
Ämneskategorier Mikrobiologi inom det medicinska området, Immunologi inom det medicinska området, Immunbiologi

Sammanfattning

Adenoviral (Ad) vaccine vectors can generate protective immunity to various pathogens in animal studies. However, recent failures in clinical vaccine trials have underscored the need for a better understanding of how mucosal immune responses to Ad-encoded vaccine Ags are generated in vivo. In this study, we addressed whether directing Ad-encoded ovalbumin (OVA) to different subcellular compartments influences the generation of OVA-specific acquired immunity and the APCs required following i.n. immunization of mice. We show that both secreted and membrane-anchored OVA activate CD4(+) T cells, induce cytotoxic CD8(+) T lymphocytes (CTLs) and generate serum IgG. Additionally, vaginal IgG is induced when OVA is expressed at these subcellular locations, but only the secreted form generates a significant IgA response in the lungs. On the contrary, intracellular expression of OVA efficiently expands CD8(+) T cells but fails to activate CD4(+) T cells, results in poor CTL activity, and does not generate Abs. Finally, we show that regardless of the subcellular localization of OVA, conventional DCs (cDCs) are required for the activation of T cells. However, the direct transduction of conventional DCs is not essential. These findings have important implications for the improvement of Ad vector design and vaccine-induced mucosal immunity.

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