pubmed-article:15784551 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15784551 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:15784551 | lifeskim:mentions | umls-concept:C0021764 | lld:lifeskim |
pubmed-article:15784551 | lifeskim:mentions | umls-concept:C0221198 | lld:lifeskim |
pubmed-article:15784551 | lifeskim:mentions | umls-concept:C0023277 | lld:lifeskim |
pubmed-article:15784551 | lifeskim:mentions | umls-concept:C2699488 | lld:lifeskim |
pubmed-article:15784551 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:15784551 | pubmed:dateCreated | 2005-3-23 | lld:pubmed |
pubmed-article:15784551 | pubmed:abstractText | Infection of C57BL/6 (B6) mice with Leishmania mexicana is associated with a minimal immune response and chronic disease. Here we show that B6 interleukin 10-/- (IL-10-/-) mice resolve their lesions and exhibit increased gamma interferon (IFN-gamma), nitric oxide production, and delayed-type hypersensitivity. This enhanced resistance was dependent upon IL-12p40, since treatment of L. mexicana-infected IL-10-/- mice with anti-IL-12p40 monoclonal antibody abrogated healing. Antibody-opsonized L. mexicana induced IL-10 production by B6 macrophages in vitro, implicating antibody binding to Fc receptors as a mechanism involved in IL-10 production in this infection. Furthermore, B6 FcRgamma-/- mice resolve L. mexicana lesions, and lymph node cells from these mice produced less IL-10 and more IFN-gamma than cells from infected wild-type mice. These data demonstrate that removal of IL-10 or FcgammaR leads to resolution of L. mexicana disease and support a model in which ligation of FcgammaR by L. mexicana-bound immunoglobulin G promotes IL-10 production, leading to chronic disease. | lld:pubmed |
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pubmed-article:15784551 | pubmed:language | eng | lld:pubmed |
pubmed-article:15784551 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15784551 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:15784551 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15784551 | pubmed:month | Apr | lld:pubmed |
pubmed-article:15784551 | pubmed:issn | 0019-9567 | lld:pubmed |
pubmed-article:15784551 | pubmed:author | pubmed-author:ScottPhillipP | lld:pubmed |
pubmed-article:15784551 | pubmed:author | pubmed-author:BuxbaumLauren... | lld:pubmed |
pubmed-article:15784551 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15784551 | pubmed:volume | 73 | lld:pubmed |
pubmed-article:15784551 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15784551 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15784551 | pubmed:pagination | 2101-8 | lld:pubmed |
pubmed-article:15784551 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:15784551 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:15784551 | pubmed:articleTitle | Interleukin 10- and Fcgamma receptor-deficient mice resolve Leishmania mexicana lesions. | lld:pubmed |
pubmed-article:15784551 | pubmed:affiliation | Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, 216 ROS, 3800 Spruce Street, Philadelphia, PA 19104, USA. | lld:pubmed |
pubmed-article:15784551 | pubmed:publicationType | Journal Article | lld:pubmed |