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Critical Reviews™ in Immunology
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ISSN Imprimir: 1040-8401
ISSN En Línea: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v25.i5.40
pages 389-403

Molecular Interactions Between Dendritic Cells and Salmonella: Escape from Adaptive Immunity and Implications on Pathogenesis

Susan M. Bueno
Millennium Institute on Immunology and Immunotherapy, Departamento de Genetica Molecular y Microbiologia, Facultad de Ciencias Biologicas, Pontificia Universidad Catolica de Chile, Santiago, Chile; INSERM U1064, Nantes, France
Jaime A. Tobar
Departamento de Genetica Molecular y Microbiologia, Facultad de Ciencias Biologicas
Mirentxu I. Iruretagoyena
Departamento de Genetica Molecular y Microbiologia, Facultad de Ciencias Biologicas
Alexis M. Kalergis
Millennium Institute on Immunology and Immunotherapy, Departamento de Genetica Molecular y Microbiologia, Facultad de Ciencias Biologicas, Pontificia Universidad Catolica de Chile, Santiago, Chile; Departamento de Inmunologia, Facultad de Madicina

SINOPSIS

Dendritic cells (DCs) constitute the link between innate and adaptive immunity by directly recognizing pathogen-associated molecular patterns (PAMPs) on bacteria and by processing and presenting bacterial antigens to T cells. Recognition of PAMPs renders DCs as professional antigen-presenting cells with the ability to prime naive T cells and to initiate the adaptive immune response against pathogen-derived antigens. For this reason, any interference with DC function might be advantageous for bacterial survival and dissemination. Identification of the molecular interactions occurring between DCs and bacterial pathogens is necessary to understand the mechanisms that virulent bacteria have evolved to prevent recognition by the adaptive immune system. This could be helpful in the identification of possible new targets that might lead to the design of effective therapies aimed at preventing or treating serious infections by these pathogens. In this article, we focus on Salmonella enterica serovar Typhimurium, the causative agent of typhoid-like disease in the mouse, and how it is able to escape from DC-mediated antigen presentation by avoiding lysosomal degradation. This feature of virulent Salmonella requires the functional expression of the Type Three Secretion System (TTSS) and effector proteins encoded within the Salmonella pathogenicity island 2 (SPI-2). Recent studies have demonstrated that impairment of DC function by the activity of SPI-2 gene products is crucial for Salmonella pathogenesis.


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