HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Neild, A. L. Articles by Roy, C. R. Search for Related Content PubMed PubMed Citation Articles by Neild, A. L. Articles by Roy, C. R. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Substance via MeSH

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.

This article has been cited by other articles:

				U. Bhan, G. Trujillo, K. Lyn-Kew, M. W. Newstead, X. Zeng, C. M. Hogaboam, A. M. Krieg, and T. J. Standiford Toll-Like Receptor 9 Regulates the Lung Macrophage Phenotype and Host Immunity in Murine Pneumonia Caused by Legionella pneumophila Infect. Immun., July 1, 2008; 76(7): 2895 - 2904. [Abstract] [Full Text] [PDF]

				A. W. M. van der Velden, J. T. Dougherty, and M. N. Starnbach Down-Modulation of TCR Expression by Salmonella enterica serovar Typhimurium J. Immunol., April 15, 2008; 180(8): 5569 - 5574. [Abstract] [Full Text] [PDF]

				M. D. Woolard, J. E. Wilson, L. L. Hensley, L. A. Jania, T. H. Kawula, J. R. Drake, and J. A. Frelinger Francisella tularensis-Infected Macrophages Release Prostaglandin E2 that Blocks T Cell Proliferation and Promotes a Th2-Like Response J. Immunol., February 15, 2007; 178(4): 2065 - 2074. [Abstract] [Full Text] [PDF]

				P. D. N'Guessan, M. O. Etouem, B. Schmeck, A. C. Hocke, S. Scharf, K. Vardarova, B. Opitz, A. Flieger, N. Suttorp, and S. Hippenstiel Legionella pneumophila-induced PKC{alpha}-, MAPK-, and NF-{kappa}B-dependent COX-2 expression in human lung epithelium Am J Physiol Lung Cell Mol Physiol, January 1, 2007; 292(1): L267 - L277. [Abstract] [Full Text] [PDF]

				K. A. Archer and C. R. Roy MyD88-Dependent Responses Involving Toll-Like Receptor 2 Are Important for Protection and Clearance of Legionella pneumophila in a Mouse Model of Legionnaires' Disease. Infect. Immun., June 1, 2006; 74(6): 3325 - 3333. [Abstract] [Full Text] [PDF]

				R. Sporri, N. Joller, U. Albers, H. Hilbi, and A. Oxenius MyD88-Dependent IFN-{gamma} Production by NK Cells Is Key for Control of Legionella pneumophila Infection J. Immunol., May 15, 2006; 176(10): 6162 - 6171. [Abstract] [Full Text] [PDF]