IgG keeps virulent Salmonella from evading dendritic cell uptake
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submitted by acintiomlivo 2 months ago
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DCs are phagocytic professional antigen presenting cells that can prime naïve T cells and initiate anti-bacterial immunity. However, several pathogenic bacteria have developed virulence mechanisms to impair DC function. For instance, Salmonella enterica serovar Typhimurium can prevent DCs from activating antigen-specific T cells. In addition, it has been described that the Salmonella Pathogenicity Island 1 (SPI-1), which promotes phagocytosis of bacteria in non-phagocytic cells, can suppresses this process in DCs in a PI3K-dependent manner. Both mechanisms allow Salmonella to evade host adaptive immunity. Recent studies have shown that IgG-opsonization of Salmonella can restore the capacity of DCs to present antigenic pMHC complexes and prime T cells. Interestingly, T cell activation requires FcγRIII expression over DCs surface, suggesting that this receptor could counteract both antigen presentation and phagocytosis evasion by bacteria. Here we show that, despite IgG-coated Salmonella retains its capacity to secrete anti-capture proteins, DCs are efficiently capable to engulf high load of IgG-coated bacteria. These results suggest that DCs employ another mechanism to engulf IgG-coated Salmonella, different from that used for free bacteria. In this context, we noted that DCs do not employ PI3K, actin cytoskeleton or dynamin to capture IgG-coated bacteria. Likewise, we observed that the capture is an FcγR-independent mechanism. Interestingly, these internalized bacteria were rapidly targeted for degradation within lysosomal compartments. Thus, our results suggest a novel mechanism in DCs that does not employ PI3K/actin cytoskeleton/dynamin/FcγRs to engulf IgG-coated Salmonella, is not affected by anti-capture SPI-1-derived effectors and enhance DC immunogenicity, bacterial degradation and antigen presentation.
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