Source:http://linkedlifedata.com/resource/pubmed/id/20956351
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
|
| pubmed:dateCreated |
2010-11-4
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| pubmed:abstractText |
Interleukin-17A-producing T cells, especially Th17, have been shown to be involved in inflammatory autoimmune diseases and host defense against extracellular infections. However, whether and how IL-17A or IL-17A-producing cells can help protection against intracellular bacteria remains controversial, especially how it regulates the adaptive immunity besides recruitment of neutrophils in the innate immune system. By infecting IL-17A-deficient mice with Listeria monocytogenes, we show in this study that IL-17A is required for the generation of Ag-specific CD8(+) CTL response against primary infection, but not for the generation of memory CD8(+) T cells against secondary challenge. Interestingly, we identify ??T cells, but not conventional CD4(+) Th17 cells, as the main cells for innate IL-17A production during L. monocytogenes infection. Furthermore, ??T cells are found to promote Ag-specific CD8(+) T cell proliferation by enhancing cross-presentation of dendritic cells through IL-17A. Adoptive transfer of Il17a(+/+) ??T cells, but not Il17a(-/-) ??T cells or Il17a(+/+) CD4(+) T cells, were sufficient to recover dendritic cells cross-presentation and defective CD8(+) T cell response in Il17a(-/-) mice. Our findings indicate an important role of infection-inducible IL-17A-producing ??T cells and their derived IL-17A against intracellular bacterial infection, providing a mechanism of IL-17A for regulation of innate and adaptive immunity.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Nov
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| pubmed:issn |
1550-6606
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| pubmed:author | |
| pubmed:issnType |
Electronic
|
| pubmed:day |
15
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| pubmed:volume |
185
|
| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
5879-87
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| pubmed:meshHeading |
pubmed-meshheading:20956351-Adoptive Transfer,
pubmed-meshheading:20956351-Animals,
pubmed-meshheading:20956351-CD8-Positive T-Lymphocytes,
pubmed-meshheading:20956351-Cell Separation,
pubmed-meshheading:20956351-Cross-Priming,
pubmed-meshheading:20956351-Cytotoxicity, Immunologic,
pubmed-meshheading:20956351-Dendritic Cells,
pubmed-meshheading:20956351-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:20956351-Flow Cytometry,
pubmed-meshheading:20956351-Interleukin-17,
pubmed-meshheading:20956351-Listeria monocytogenes,
pubmed-meshheading:20956351-Listeriosis,
pubmed-meshheading:20956351-Mice,
pubmed-meshheading:20956351-Mice, Inbred C57BL,
pubmed-meshheading:20956351-Mice, Knockout,
pubmed-meshheading:20956351-Receptors, Antigen, T-Cell, gamma-delta,
pubmed-meshheading:20956351-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:20956351-T-Lymphocyte Subsets,
pubmed-meshheading:20956351-Th17 Cells
|
| pubmed:year |
2010
|
| pubmed:articleTitle |
IL-17A-producing gammadeltaT cells promote CTL responses against Listeria monocytogenes infection by enhancing dendritic cell cross-presentation.
|
| pubmed:affiliation |
National Key Laboratory of Medical Immunology, Second Military Medical University, Shanghai, China.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|