• Medientyp: E-Artikel
  • Titel: Mechanisms used by virulent Salmonella to impair dendritic cell function and evade adaptive immunity
  • Beteiligte: Bueno, Susan M.; Riquelme, Sebastián; Riedel, Claudia A.; Kalergis, Alexis M.
  • Erschienen: Wiley, 2012
  • Erschienen in: Immunology
  • Umfang: 28-36
  • Sprache: Englisch
  • DOI: 10.1111/j.1365-2567.2012.03614.x
  • ISSN: 0019-2805; 1365-2567
  • Schlagwörter: Immunology ; Immunology and Allergy
  • Zusammenfassung: <jats:title>Summary</jats:title><jats:p>Innate and adaptive immunity are inter‐related by dendritic cells (<jats:styled-content style="fixed-case">DC</jats:styled-content>s), which directly recognize bacteria through the binding of pathogen‐associated molecular patterns (<jats:styled-content style="fixed-case">PAMP</jats:styled-content>s) to specialized receptors on their surface. After capturing and degrading bacteria, <jats:styled-content style="fixed-case">DC</jats:styled-content>s present their antigens as small peptides bound to <jats:styled-content style="fixed-case">MHC</jats:styled-content> molecules and prime naive bacteria‐specific T cells. In response to <jats:styled-content style="fixed-case">PAMP</jats:styled-content> recognition <jats:styled-content style="fixed-case">DC</jats:styled-content>s undergo maturation, which is a phenotypic change that increases their immunogenicity and promotes the activation of naive T cells. As a result, a specific immune response that targets bacteria‐derived antigens is initiated. Therefore, the characterization of <jats:styled-content style="fixed-case">DC</jats:styled-content>–bacteria interactions is important to understand the mechanisms used by virulent bacteria to avoid adaptive immunity. Furthermore, any impairment of <jats:styled-content style="fixed-case">DC</jats:styled-content> function might contribute to bacterial survival and dissemination inside the host. An example of a bacterial pathogen capable of interfering with <jats:styled-content style="fixed-case">DC</jats:styled-content> function is <jats:italic>Salmonella enterica</jats:italic> serovar Typhimurium (<jats:italic>S</jats:italic>. Typhimurium). Virulent strains of this bacterium are able to differentially modulate the entrance to <jats:styled-content style="fixed-case">DC</jats:styled-content>s, avoid lysosomal degradation and prevent antigen presentation on <jats:styled-content style="fixed-case">MHC</jats:styled-content> molecules. These features of virulent <jats:italic>S. </jats:italic>Typhimurium are controlled by virulence proteins, which are encoded by pathogenicity islands. Modulation of <jats:styled-content style="fixed-case">DC</jats:styled-content> functions by these gene products is supported by several studies showing that pathogenesis might depend on this attribute of virulent <jats:italic>S. </jats:italic>Typhimurium. Here we discuss some of the recent data reported by the literature showing that several virulence proteins from <jats:italic>Salmonella</jats:italic> are required to modulate <jats:styled-content style="fixed-case">DC</jats:styled-content> function and the activation of host adaptive immunity.</jats:p>
  • Beschreibung: <jats:title>Summary</jats:title><jats:p>Innate and adaptive immunity are inter‐related by dendritic cells (<jats:styled-content style="fixed-case">DC</jats:styled-content>s), which directly recognize bacteria through the binding of pathogen‐associated molecular patterns (<jats:styled-content style="fixed-case">PAMP</jats:styled-content>s) to specialized receptors on their surface. After capturing and degrading bacteria, <jats:styled-content style="fixed-case">DC</jats:styled-content>s present their antigens as small peptides bound to <jats:styled-content style="fixed-case">MHC</jats:styled-content> molecules and prime naive bacteria‐specific T cells. In response to <jats:styled-content style="fixed-case">PAMP</jats:styled-content> recognition <jats:styled-content style="fixed-case">DC</jats:styled-content>s undergo maturation, which is a phenotypic change that increases their immunogenicity and promotes the activation of naive T cells. As a result, a specific immune response that targets bacteria‐derived antigens is initiated. Therefore, the characterization of <jats:styled-content style="fixed-case">DC</jats:styled-content>–bacteria interactions is important to understand the mechanisms used by virulent bacteria to avoid adaptive immunity. Furthermore, any impairment of <jats:styled-content style="fixed-case">DC</jats:styled-content> function might contribute to bacterial survival and dissemination inside the host. An example of a bacterial pathogen capable of interfering with <jats:styled-content style="fixed-case">DC</jats:styled-content> function is <jats:italic>Salmonella enterica</jats:italic> serovar Typhimurium (<jats:italic>S</jats:italic>. Typhimurium). Virulent strains of this bacterium are able to differentially modulate the entrance to <jats:styled-content style="fixed-case">DC</jats:styled-content>s, avoid lysosomal degradation and prevent antigen presentation on <jats:styled-content style="fixed-case">MHC</jats:styled-content> molecules. These features of virulent <jats:italic>S. </jats:italic>Typhimurium are controlled by virulence proteins, which are encoded by pathogenicity islands. Modulation of <jats:styled-content style="fixed-case">DC</jats:styled-content> functions by these gene products is supported by several studies showing that pathogenesis might depend on this attribute of virulent <jats:italic>S. </jats:italic>Typhimurium. Here we discuss some of the recent data reported by the literature showing that several virulence proteins from <jats:italic>Salmonella</jats:italic> are required to modulate <jats:styled-content style="fixed-case">DC</jats:styled-content> function and the activation of host adaptive immunity.</jats:p>
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