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Nontyphoidal serovars ofSalmonella enterica are pathogenic bacteria that are common causes of food poisoning. WhereasSalmonella mechanisms of host cell invasion, inflammation, and pathogenesis are mostly well established, a new possible mechanism of immune evasion is being uncovered. Programmed death ligand 1 (PD-L1) is an immunosuppressive membrane protein that binds to activated T cells via their PD-1 receptor and thereby halts their activation. PD-L1 expression plays an essential role in the immunological tolerance of self-antigens but is also exploited for immune evasion by pathogen-infected cells and cancer cells. Here, we show for the first time thatSalmonella infection of intestinal epithelial cells causes the induction of PD-L1. The increased expression of PD-L1 throughSalmonella infection was seen in both human and rat intestinal epithelial cell lines. We determined that cellular invasion by the bacteria is necessary for PD-L1 induction, potentially indicating thatSalmonella strains are delivering mediators from inside the host cell that trigger the increased PD-L1 expression. Using knockout mutants, we determined that this effect largely originates from theSalmonella pathogenicity island 2. We also show for the first time in any cell type thatSalmonella combined with gamma interferon (IFN-γ) causes a synergistic induction of PD-L1. Finally, we show thatSalmonella plus IFN-γ induction of PD-L1 decreased the cytokine production of activated T cells. UnderstandingSalmonella immune evasion strategies could generate new therapeutic targets and help to manipulate PD-L1 expression in other diseases.

infection and immunity

Salmonella enterica Serovar Typhimurium Increases Functional PD-L1 Synergistically with Gamma Interferon in Intestinal Epithelial Cells via Salmonella Pathogenicity Island 2