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    An SopB-mediated immune escape mechanism of Salmonella enterica can be subverted to optimize the performance of live attenuated vaccine carrier strains.

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    Authors
    Link, Claudia
    Ebensen, Thomas
    Ständner, Lothar
    Déjosez, Marion
    Reinhard, Elena
    Rharbaoui, Faiza
    Guzmán, Carlos A
    Issue Date
    2006-07
    
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    Abstract
    Salmonellae have evolved several mechanisms to evade host clearance. Here, we describe the influence on bacterial immune escape of the effector protein SopB, which is translocated into the cytosol through a type III secretion system. Wild-type bacteria, as well as the sseC and aroA attenuated mutants exerted a stronger cytotoxic effect on dendritic cells (DC) than their SopB-deficient derivatives. Cells infected with the double sseC sopB, phoP sopB and aroA sopB mutants also exhibited higher expression of MHC, CD80, CD86 and CD54 molecules, and showed a stronger capacity to process and present an I-E(d)-restricted epitope from the influenza hemagglutinin (HA) to CD4+ cells from TCR-HA transgenic mice in vitro. The incorporation of an additional mutation into the sopB locus of the attenuated sseC, phoP and aroA mutants resulted in the stimulation of improved humoral and cellular immune responses following oral vaccination. The obtained results define a new potential immune escape strategy of this important pathogen, and also demonstrate that this mechanism can be subverted to optimize the immune responses elicited using Salmonella as a live vaccine carrier.
    Citation
    An SopB-mediated immune escape mechanism of Salmonella enterica can be subverted to optimize the performance of live attenuated vaccine carrier strains. 2006, 8 (8):2262-9 Microbes Infect.
    Affiliation
    Department of Vaccinology, Division of Microbiology, GBF-German Research Centre for Biotechnology, Mascheroder Weg 1, D-38124 Braunschweig, Germany.
    Journal
    Microbes and infection / Institut Pasteur
    URI
    http://hdl.handle.net/10033/15913
    DOI
    10.1016/j.micinf.2006.04.013
    PubMed ID
    16793312
    Type
    Article
    Language
    en
    ISSN
    1286-4579
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.micinf.2006.04.013
    Scopus Count
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    publications of the research group vaccinology and applied microbiology (VAC)

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