Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2002-6-10
pubmed:abstractText
Host resistance to the intracellular protozoan Toxoplasma gondii is highly dependent on early IL-12 production by APC. We demonstrate here that both host resistance and T. gondii-induced IL-12 production are dramatically reduced in mice lacking the adaptor molecule MyD88, an important signaling element used by Toll-like receptor (TLR) family members. Infection of MyD88-deficient mice with T. gondii resulted in uncontrolled parasite replication and greatly reduced plasma IL-12 levels. Defective IL-12 responses to T. gondii Ags (soluble tachyzoite Ag (STAg)) were observed in MyD88(-/-) peritoneal macrophages, neutrophils, and splenic dendritic cells (DC). In contrast, DC from TLR2- or TLR4-deficient animals developed normal IL-12 responses to STAg. In vivo treatment with pertussis toxin abolished the residual IL-12 response displayed by STAg-stimulated DC from MyD88(-/-) mice. Taken together, these data suggest that the induction of IL-12 by T. gondii depends on a unique mechanism involving both MyD88 and G protein-coupled signaling pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Signal Transducing, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation, http://linkedlifedata.com/resource/pubmed/chemical/Drosophila Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins, 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/Receptors, CCR5, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 2, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 4, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
168
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5997-6001
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:12055206-Adaptor Proteins, Signal Transducing, pubmed-meshheading:12055206-Animals, pubmed-meshheading:12055206-Antigens, Differentiation, pubmed-meshheading:12055206-Dendritic Cells, pubmed-meshheading:12055206-Drosophila Proteins, pubmed-meshheading:12055206-Female, pubmed-meshheading:12055206-Immunity, Innate, pubmed-meshheading:12055206-Interferon-gamma, pubmed-meshheading:12055206-Interleukin-12, pubmed-meshheading:12055206-Macrophages, Peritoneal, pubmed-meshheading:12055206-Male, pubmed-meshheading:12055206-Membrane Glycoproteins, pubmed-meshheading:12055206-Mice, pubmed-meshheading:12055206-Mice, Inbred C57BL, pubmed-meshheading:12055206-Mice, Knockout, pubmed-meshheading:12055206-Myeloid Differentiation Factor 88, pubmed-meshheading:12055206-Neutrophils, pubmed-meshheading:12055206-Receptors, CCR5, pubmed-meshheading:12055206-Receptors, Cell Surface, pubmed-meshheading:12055206-Receptors, Immunologic, pubmed-meshheading:12055206-Signal Transduction, pubmed-meshheading:12055206-Toll-Like Receptor 2, pubmed-meshheading:12055206-Toll-Like Receptor 4, pubmed-meshheading:12055206-Toll-Like Receptors, pubmed-meshheading:12055206-Toxoplasma, pubmed-meshheading:12055206-Toxoplasmosis, Animal
pubmed:year
2002
pubmed:articleTitle
Cutting edge: MyD88 is required for resistance to Toxoplasma gondii infection and regulates parasite-induced IL-12 production by dendritic cells.
pubmed:affiliation
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. cscanga@niaid.nih.gov
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't