Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2006-11-3
pubmed:abstractText
Host resistance to the intracellular protozoan parasite Trypanosoma cruzi depends on IFN-gamma production by T cells and NK cells. However, the involvement of innate immunity in host resistance to T. cruzi remains unclear. In the present study, we investigated host defense against T. cruzi by focusing on innate immunity. Macrophages and dendritic cells (DCs) from MyD88(-/-)TRIF(-/-) mice, in which TLR-dependent activation of innate immunity was abolished, were defective in the clearance of T. cruzi and showed impaired induction of IFN-beta during T. cruzi infection. Neutralization of IFN-beta in MyD88(-/-) macrophages led to enhanced T. cruzi growth. Cells from MyD88(-/-)IFNAR1(-/-) mice also showed impaired T. cruzi clearance. Furthermore, both MyD88(-/-)TRIF(-/-) and MyD88(-/-)IFNAR1(-/-) mice were highly susceptible to in vivo T. cruzi infection, highlighting the involvement of innate immune responses in T. cruzi infection. We further analyzed the molecular mechanisms for the IFN-beta-mediated antitrypanosomal innate immune responses. MyD88(-/-)TRIF(-/-) and MyD88(-/-)IFNAR1(-/-) macrophages and DCs exhibited defective induction of the GTPase IFN-inducible p47 (IRG47) after T. cruzi infection. RNA interference-mediated reduction of IRG47 expression in MyD88(-/-) macrophages resulted in increased intracellular growth of T. cruzi. These findings suggest that TLR-dependent expression of IFN-beta is involved in resistance to T. cruzi infection through the induction of IRG47.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Vesicular..., http://linkedlifedata.com/resource/pubmed/chemical/GTP Phosphohydrolases, http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Growth Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Ifi1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Ifnar1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators, http://linkedlifedata.com/resource/pubmed/chemical/Interferon-beta, http://linkedlifedata.com/resource/pubmed/chemical/Myd88 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Myeloid Differentiation Factor 88, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Interferon alpha-beta, http://linkedlifedata.com/resource/pubmed/chemical/TICAM-1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
177
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7059-66
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17082622-Adaptor Proteins, Vesicular Transport, pubmed-meshheading:17082622-Animals, pubmed-meshheading:17082622-Cells, Cultured, pubmed-meshheading:17082622-Chagas Disease, pubmed-meshheading:17082622-Dendritic Cells, pubmed-meshheading:17082622-GTP Phosphohydrolases, pubmed-meshheading:17082622-GTP-Binding Proteins, pubmed-meshheading:17082622-Gene Expression Regulation, pubmed-meshheading:17082622-Growth Inhibitors, pubmed-meshheading:17082622-Immunity, Innate, pubmed-meshheading:17082622-Inflammation Mediators, pubmed-meshheading:17082622-Interferon-beta, pubmed-meshheading:17082622-Macrophages, Peritoneal, pubmed-meshheading:17082622-Mice, pubmed-meshheading:17082622-Mice, Inbred C57BL, pubmed-meshheading:17082622-Mice, Knockout, pubmed-meshheading:17082622-Myeloid Differentiation Factor 88, pubmed-meshheading:17082622-Receptor, Interferon alpha-beta, pubmed-meshheading:17082622-Toll-Like Receptors, pubmed-meshheading:17082622-Trypanosoma cruzi
pubmed:year
2006
pubmed:articleTitle
TLR-dependent induction of IFN-beta mediates host defense against Trypanosoma cruzi.
pubmed:affiliation
Department of Molecular Genetics, Medical Institute of Bioregulation, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't