Source:http://linkedlifedata.com/resource/pubmed/id/20231435
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
13
|
| pubmed:dateCreated |
2010-4-1
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| pubmed:abstractText |
Recurrent group A Streptococcus (GAS) tonsillitis and associated autoimmune diseases indicate that the immune response to this organism can be ineffective and pathological. TGF-beta1 is recognized as an essential signal for generation of regulatory T cells (Tregs) and T helper (Th) 17 cells. Here, the impact of TGF-beta1 induction on the T-cell response in mouse nasal-associated lymphoid tissue (NALT) following intranasal (i.n.) infections is investigated. ELISA and TGF-beta1-luciferase reporter assays indicated that persistent infection of mouse NALT with GAS sets the stage for TGF-beta1 and IL-6 production, signals required for promotion of a Th17 immune response. As predicted, IL-17, the Th17 signature cytokine, was induced in a TGF-beta1 signaling-dependent manner in single-cell suspensions of both human tonsils and NALT. Intracellular cytokine staining and flow cytometry demonstrated that CD4(+) IL-17(+) T cells are the dominant T cells induced in NALT by i.n. infections. Moreover, naive mice acquired the potential to clear GAS by adoptive transfer of CD4(+) T cells from immunized IL-17A(+)/(+) mice but not cells from IL-17A(-)/(-) mice. These experiments link specific induction of TGF-beta1 by a bacterial infection to an in vivo Th17 immune response and show that this cellular response is sufficient for protection against GAS. The association of a Th17 response with GAS infection reveals a potential mechanism for destructive autoimmune responses in humans.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Mar
|
| pubmed:issn |
1091-6490
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
30
|
| pubmed:volume |
107
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
5937-42
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:20231435-Animals,
pubmed-meshheading:20231435-Cell Differentiation,
pubmed-meshheading:20231435-Cytokines,
pubmed-meshheading:20231435-Female,
pubmed-meshheading:20231435-Humans,
pubmed-meshheading:20231435-Immunity, Cellular,
pubmed-meshheading:20231435-Interleukin-17,
pubmed-meshheading:20231435-Listeria monocytogenes,
pubmed-meshheading:20231435-Listeriosis,
pubmed-meshheading:20231435-Lymphoid Tissue,
pubmed-meshheading:20231435-Mice,
pubmed-meshheading:20231435-Mice, Inbred BALB C,
pubmed-meshheading:20231435-Mice, Inbred C57BL,
pubmed-meshheading:20231435-Mice, Knockout,
pubmed-meshheading:20231435-Nasal Cavity,
pubmed-meshheading:20231435-Signal Transduction,
pubmed-meshheading:20231435-Streptococcal Infections,
pubmed-meshheading:20231435-Streptococcus pyogenes,
pubmed-meshheading:20231435-T-Lymphocyte Subsets,
pubmed-meshheading:20231435-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:20231435-Th1 Cells,
pubmed-meshheading:20231435-Tonsillitis,
pubmed-meshheading:20231435-Transforming Growth Factor beta1
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| pubmed:year |
2010
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| pubmed:articleTitle |
Induction of TGF-beta1 and TGF-beta1-dependent predominant Th17 differentiation by group A streptococcal infection.
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| pubmed:affiliation |
Department of Microbiology, and Discovery Genomics, Inc, Minneapolis, MN 55413, USA. wangx351@umn.edu
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| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
|