Source:http://linkedlifedata.com/resource/pubmed/id/17513774
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
2007-5-21
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pubmed:abstractText |
Protection against Leishmania major in resistant C57BL/6 mice is mediated by Th1 cells, whereas susceptibility in BALB/c mice is the result of Th2 development. IL-12 release by L. major-infected dendritic cells (DC) is critically involved in differentiation of Th1 cells. Previously, we reported that strain differences in the production of DC-derived factors, e.g., IL-1alphabeta, are in part responsible for disparate disease outcome. In the present study, we analyzed the release of IL-12 from DC in more detail. Stimulated DC from C57BL/6 and BALB/c mice released comparable amounts of IL-12p40 and p70. In the absence of IL-4, BALB/c DC produced significantly more IL-12p40 than C57BL/6 DC. Detailed analyses by Western blot and ELISA revealed that one-tenth of IL-12p40 detected in DC supernatants was released as the IL-12 antagonist IL-12p40 homodimer (IL-12p80). BALB/c DC released approximately 2-fold more IL-12p80 than C57BL/6 DC both in vitro and in vivo. Local injection of IL-12p80 during the first 3 days after infection resulted in increased lesion volumes for several weeks in both L. major-infected BALB/c or C57BL/6 mice, in higher lesional parasite burdens, and decreased Th1-cytokine production. Finally, IL-12p40-transgenic C57BL/6 mice characterized by overexpression of p40 showed increased levels of serum IL-12p80 and enhanced disease susceptibility. Thus, in addition to IL-1alphabeta, strain-dependent differences in the release of other DC-derived factors such as IL-12p80 may influence genetically determined disease outcome.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
178
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7251-8
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17513774-Animals,
pubmed-meshheading:17513774-Cells, Cultured,
pubmed-meshheading:17513774-Dendritic Cells,
pubmed-meshheading:17513774-Dimerization,
pubmed-meshheading:17513774-Genetic Predisposition to Disease,
pubmed-meshheading:17513774-Immunity, Innate,
pubmed-meshheading:17513774-Interleukin-12,
pubmed-meshheading:17513774-Interleukin-12 Subunit p40,
pubmed-meshheading:17513774-Interleukin-4,
pubmed-meshheading:17513774-Leishmania major,
pubmed-meshheading:17513774-Leishmaniasis, Cutaneous,
pubmed-meshheading:17513774-Mice,
pubmed-meshheading:17513774-Mice, Inbred BALB C,
pubmed-meshheading:17513774-Mice, Inbred C57BL,
pubmed-meshheading:17513774-Mice, Transgenic,
pubmed-meshheading:17513774-Signal Transduction,
pubmed-meshheading:17513774-Species Specificity
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pubmed:year |
2007
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pubmed:articleTitle |
Dendritic cell-derived IL-12p40 homodimer contributes to susceptibility in cutaneous leishmaniasis in BALB/c mice.
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pubmed:affiliation |
Department of Dermatology, Johannes Gutenberg-University, Mainz, Germany.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Intramural
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