| First Author | Neild AL | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 12 | Pages | 8181-90 |
| PubMed ID | 16339557 | Mgi Jnum | J:122277 |
| Mgi Id | MGI:3713949 | Doi | 10.4049/jimmunol.175.12.8181 |
| Citation | Neild AL, et al. (2005) Activated macrophages infected with Legionella inhibit T cells by means of MyD88-dependent production of prostaglandins. J Immunol 175(12):8181-90 |
| abstractText | To understand how macrophages (Mphi) activated with IFN-gamma modulate the adaptive immune response to intracellular pathogens, the interaction of IFN-gamma-treated bone marrow-derived murine Mphi (BMphi) 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-gamma-treated BMphi, intracellular growth of Legionella was restricted. It was determined that activated BMphi infected with Legionella suppressed IFN-gamma 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 BMphi following Legionella infection. Signaling pathways requiring MyD88 and TLR2 were important for production of a factor produced by IFN-gamma-treated BMphi that interfered with effector T cell functions. Cyclooxygenase-2-dependent production of PGs by IFN-gamma-treated BMphi infected with Legionella was required for inhibition of effector T cell responses. From these data we conclude that activated Mphi 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. |
