TLR9 activation is a key event for the maintenance of a mycobacterial antigen-elicited pulmonary granulomatous response

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dc.contributor.author Ito, Toshihiro en_US
dc.contributor.author Schaller, Matthew en_US
dc.contributor.author Hogaboam, Cory M. en_US
dc.contributor.author Standiford, Theodore J. en_US
dc.contributor.author Chensue, Stephen W. en_US
dc.date.accessioned 2007-12-04T18:25:32Z
dc.date.available 2008-11-05T15:05:43Z en_US
dc.date.issued 2007-10 en_US
dc.identifier.citation Ito, Toshihiro; Schaller, Matthew; Hogaboam, Cory M.; Standiford, Theodore J.; Chensue, Stephen W. (2007). "TLR9 activation is a key event for the maintenance of a mycobacterial antigen-elicited pulmonary granulomatous response." European Journal of Immunology 37(10): 2847-2855. <http://hdl.handle.net/2027.42/57331> en_US
dc.identifier.issn 0014-2980 en_US
dc.identifier.issn 1521-4141 en_US
dc.identifier.uri http://hdl.handle.net/2027.42/57331
dc.identifier.uri http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17853411&dopt=citation
dc.description.abstract Type 1 (Th1) granulomas can be studied in mice sensitized with mycobacterium antigens followed by challenge of agarose beads covalently coupled to purified protein derivative. TLR9 is known to play a role in the regulation of Th1 responses; thus, we investigated the role of TLR9 in granuloma formation during challenge with mycobacterium antigens and demonstrated that mice deficient in TLR9 had increased granuloma formation, but a dramatically altered cytokine phenotype. Th1 cytokine levels of IFN-γ and IL-12 in the lungs were decreased in TLR9 –/– mice when compared to wild-type mice. In contrast, Th2 cytokine levels of IL-4, IL-5, and IL-13 were increased in TLR9 –/– mice. The migration of CD4 + T cells in the granuloma was impaired, while the number of F4/80 + macrophages was increased in TLR9 –/– mice. Macrophages in the lungs of the TLR9-deficient animals with developing granulomas expressed significantly lower levels of the classically activated macrophage marker, nitric oxide synthase, but higher levels of the alternatively activated macrophage markers such as ‘found in inflammatory zone-1′ antigen and Arginase-1. These results suggest that TLR9 plays an important role in maintaining the appropriate phenotype in a Th1 granulomatous response. en_US
dc.format.extent 368177 bytes
dc.format.extent 3118 bytes
dc.format.mimetype application/pdf
dc.format.mimetype text/plain
dc.publisher WILEY-VCH Verlag en_US
dc.subject.other Life and Medical Sciences en_US
dc.subject.other Microbiology and Immunology en_US
dc.title TLR9 activation is a key event for the maintenance of a mycobacterial antigen-elicited pulmonary granulomatous response en_US
dc.type Article en_US
dc.rights.robots IndexNoFollow en_US
dc.subject.hlbsecondlevel Biological Chemistry en_US
dc.subject.hlbsecondlevel Public Health en_US
dc.subject.hlbtoplevel Health Sciences en_US
dc.subject.hlbtoplevel Science en_US
dc.description.peerreviewed Peer Reviewed en_US
dc.contributor.affiliationum Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA ; Second Department of Internal Medicine, Nara Medical University, Nara, Japan en_US
dc.contributor.affiliationum Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA en_US
dc.contributor.affiliationum Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA en_US
dc.contributor.affiliationum Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA en_US
dc.contributor.affiliationum Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA ; Department of Pathology and Laboratory Medicine, Veterans Affairs Ann Arbor Healthcare System, Ann Arbor, MI, USA en_US
dc.identifier.pmid 17853411
dc.description.bitstreamurl http://deepblue.lib.umich.edu/bitstream/2027.42/57331/1/2847_ftp.pdf en_US
dc.identifier.doi http://dx.doi.org/10.1002/eji.200737603 en_US
dc.identifier.source European Journal of Immunology en_US
dc.owningcollname Interdisciplinary and Peer-Reviewed
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