| pubmed-article:20231435 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20231435 | lifeskim:mentions | umls-concept:C0038395 | lld:lifeskim |
| pubmed-article:20231435 | lifeskim:mentions | umls-concept:C1257890 | lld:lifeskim |
| pubmed-article:20231435 | lifeskim:mentions | umls-concept:C1704256 | lld:lifeskim |
| pubmed-article:20231435 | lifeskim:mentions | umls-concept:C0007589 | lld:lifeskim |
| pubmed-article:20231435 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:20231435 | lifeskim:mentions | umls-concept:C1511938 | lld:lifeskim |
| pubmed-article:20231435 | pubmed:issue | 13 | lld:pubmed |
| pubmed-article:20231435 | pubmed:dateCreated | 2010-4-1 | lld:pubmed |
| pubmed-article:20231435 | 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. | lld:pubmed |
| pubmed-article:20231435 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20231435 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20231435 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20231435 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20231435 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20231435 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20231435 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20231435 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20231435 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:20231435 | pubmed:issn | 1091-6490 | lld:pubmed |
| pubmed-article:20231435 | pubmed:author | pubmed-author:WangBeinanB | lld:pubmed |
| pubmed-article:20231435 | pubmed:author | pubmed-author:ClearyP... | lld:pubmed |
| pubmed-article:20231435 | pubmed:author | pubmed-author:KhorutsAlexan... | lld:pubmed |
| pubmed-article:20231435 | pubmed:author | pubmed-author:KangJohnthoma... | lld:pubmed |
| pubmed-article:20231435 | pubmed:author | pubmed-author:DileepanThamo... | lld:pubmed |
| pubmed-article:20231435 | pubmed:author | pubmed-author:HylandKendra... | lld:pubmed |
| pubmed-article:20231435 | pubmed:author | pubmed-author:BriscoeSarahS | lld:pubmed |
| pubmed-article:20231435 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20231435 | pubmed:day | 30 | lld:pubmed |
| pubmed-article:20231435 | pubmed:volume | 107 | lld:pubmed |
| pubmed-article:20231435 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20231435 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20231435 | pubmed:pagination | 5937-42 | lld:pubmed |
| pubmed-article:20231435 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:meshHeading | pubmed-meshheading:20231435... | lld:pubmed |
| pubmed-article:20231435 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20231435 | pubmed:articleTitle | Induction of TGF-beta1 and TGF-beta1-dependent predominant Th17 differentiation by group A streptococcal infection. | lld:pubmed |
| pubmed-article:20231435 | pubmed:affiliation | Department of Microbiology, and Discovery Genomics, Inc, Minneapolis, MN 55413, USA. wangx351@umn.edu | lld:pubmed |
| pubmed-article:20231435 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20231435 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:16171 | entrezgene:pubmed | pubmed-article:20231435 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:20231435 | lld:pubmed |
