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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2009-2-23
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pubmed:abstractText |
Resistance to leishmaniasis in C57BL/6 mice depends on Th1/Tc1 cells. BALB/c mice preferentially develop Th2 immunity and succumb to infection. We now assessed the role of IL-17 in cutaneous leishmaniasis. During the course of Leishmania major infection, BALB/c CD4 cells and neutrophils produced increased amounts of IL-17 as compared with cells from C57BL/6 mice. This increase was associated with significantly increased IL-23 release from L. major-infected BALB/c dendritic cells (DC), whereas IL-6 and TGF-beta1 production by BALB/c and C57BL/6 DC were comparable. Interestingly, lesion sizes in infected IL-17-deficient BALB/c mice were dramatically smaller and failed to progress as compared with those in control mice. Similar amounts of IL-4, IL-10, and IFN-gamma were produced by T cells from IL-17-deficient mice and control mice consistent with development of Th2-predominant immunity in all animals. Improved disease outcome was associated with decreased CXCL2-accumulation in lesion sites and decreased neutrophil immigration into lesions of infected IL-17-deficient mice confirming prior observations that enhanced neutrophil recruitment contributes to disease susceptibility in BALB/c mice. This study excludes an important facilitating role for IL-17 in Th1/Th2 development in L. major-infected BALB/c mice, and suggests that IL-23 production by L. major-infected DC maintains IL-17(+) cells that influence disease progression via regulation of neutrophil recruitment.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19234200-10946291,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19234200-11093169,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/19234200-9870666
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1550-6606
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
182
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3039-46
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pubmed:dateRevised |
2010-9-23
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pubmed:meshHeading |
pubmed-meshheading:19234200-Animals,
pubmed-meshheading:19234200-Cell Differentiation,
pubmed-meshheading:19234200-Cells, Cultured,
pubmed-meshheading:19234200-Dendritic Cells,
pubmed-meshheading:19234200-Disease Progression,
pubmed-meshheading:19234200-Genetic Predisposition to Disease,
pubmed-meshheading:19234200-Immunity, Cellular,
pubmed-meshheading:19234200-Interleukin-17,
pubmed-meshheading:19234200-Interleukin-23,
pubmed-meshheading:19234200-Leishmania major,
pubmed-meshheading:19234200-Leishmaniasis, Cutaneous,
pubmed-meshheading:19234200-Mice,
pubmed-meshheading:19234200-Mice, Inbred BALB C,
pubmed-meshheading:19234200-Mice, Inbred C57BL,
pubmed-meshheading:19234200-Mice, Knockout,
pubmed-meshheading:19234200-Neutrophils,
pubmed-meshheading:19234200-Species Specificity,
pubmed-meshheading:19234200-Th2 Cells,
pubmed-meshheading:19234200-Up-Regulation
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pubmed:year |
2009
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pubmed:articleTitle |
IL-17 promotes progression of cutaneous leishmaniasis in susceptible 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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