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Activated Macrophages Infected with Legionella Inhibit T Cells by Means of MyD88-Dependent Production of Prostaglandins¹

Yale University School of Medicine, Section of Microbial Pathogenesis, Boyer Center for Molecular Medicine, New Haven, CT 06536

To understand how macrophages (M) activated with IFN- modulate the adaptive immune response to intracellular pathogens, the interaction of IFN--treated bone marrow-derived murine M (BM) with Legionella pneumophila was investigated. Although Legionella was able to evade phagosome lysosome fusion initially, and was capable of de novo protein synthesis within IFN--treated BM, intracellular growth of Legionella was restricted. It was determined that activated BM infected with Legionella suppressed IFN- production by Ag-specific CD4 and CD8 T cells. A factor sufficient for suppression of T cell responses was present in culture supernatants isolated from activated BM following Legionella infection. Signaling pathways requiring MyD88 and TLR2 were important for production of a factor produced by IFN--treated BM that interfered with effector T cell functions. Cyclooxygenase-2-dependent production of PGs by IFN--treated BM infected with Legionella was required for inhibition of effector T cell responses. From these data we conclude that activated M can down-modulate Ag-specific T cell responses after they encounter bacterial pathogens through production of PGs, which may be important in preventing unnecessary immune-mediated damage to host tissues.

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