Abstract

Dendritic cells (DCs) are professional antigen presenting cells with the ability to recognize and degrade bacterial antigens, which are presented to naïve T cells to initiate the adaptive immune response against pathogen-derived antigens. For this reason, some bacterial pathogens have acquired virulence mechanisms that interfere with DC function and avoid the adaptive immune response activation. Salmonella enterica serovar Typhimurium, the causative agent of typhoid-like disease in the mouse, 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 other virulence proteins encoded within the Salmonella Pathogenicity Island 2 (SPI-2). In this review we discuss recent studies showing that impairment of DC function by the activity of SPI-2 gene products and the avoidance of phagosome-lysosome fusion in these cells are crucial for Salmonella pathogenesis.