| pubmed-article:17725607 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17725607 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:17725607 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:17725607 | lifeskim:mentions | umls-concept:C0041485 | lld:lifeskim |
| pubmed-article:17725607 | lifeskim:mentions | umls-concept:C0670896 | lld:lifeskim |
| pubmed-article:17725607 | lifeskim:mentions | umls-concept:C1327413 | lld:lifeskim |
| pubmed-article:17725607 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:17725607 | pubmed:dateCreated | 2008-1-14 | lld:pubmed |
| pubmed-article:17725607 | pubmed:abstractText | Bruton's tyrosine kinase (Btk), a member of the Tec family of tyrosine kinases, plays an important role in the differentiation and activation of B cells. Mutations affecting Btk cause immunodeficiency in both humans and mice. In this study we set out to investigate the potential role of Btk in Toll-like receptor 9 (TLR9) activation and the production of pro-inflammatory cytokines such as interleukin (IL)-6, tumour necrosis factor (TNF)-alpha and IL-12p40. Our data show that Btk-deficient B cells respond more efficiently to CpG-DNA stimulation, producing significantly higher levels of pro-inflammatory cytokines but lower levels of the inhibitory cytokine IL-10. The quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis presented in this work shows that mRNA production of one of the important new members of the IL-12 family, IL-27, was significantly increased in Btk-deficient B cells after CpG-DNA stimulation. In this study, we demonstrate significant differences in CpG responsiveness between transitional 1 (T1) and T2 B cells for survival and maturation. Furthermore, TLR9 expression, measured both as protein and as mRNA, was increased in Btk-defective cells, especially after TLR9 stimulation. Collectively, these data provide evidence in support of the theory that Btk regulates both TLR9 activation and expression in mouse splenic B cells. | lld:pubmed |
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| pubmed-article:17725607 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17725607 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17725607 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17725607 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17725607 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17725607 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:17725607 | pubmed:issn | 1365-2567 | lld:pubmed |
| pubmed-article:17725607 | pubmed:author | pubmed-author:SmithC I... | lld:pubmed |
| pubmed-article:17725607 | pubmed:author | pubmed-author:VargasLeonard... | lld:pubmed |
| pubmed-article:17725607 | pubmed:author | pubmed-author:LindvallJessi... | lld:pubmed |
| pubmed-article:17725607 | pubmed:author | pubmed-author:BlombergK... | lld:pubmed |
| pubmed-article:17725607 | pubmed:author | pubmed-author:BerglöfAnnaA | lld:pubmed |
| pubmed-article:17725607 | pubmed:author | pubmed-author:HasanMaroofM | lld:pubmed |
| pubmed-article:17725607 | pubmed:author | pubmed-author:Lopez-Herrera... | lld:pubmed |
| pubmed-article:17725607 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:17725607 | pubmed:volume | 123 | lld:pubmed |
| pubmed-article:17725607 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17725607 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17725607 | pubmed:pagination | 239-49 | lld:pubmed |
| pubmed-article:17725607 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
| pubmed-article:17725607 | pubmed:meshHeading | pubmed-meshheading:17725607... | lld:pubmed |
| pubmed-article:17725607 | pubmed:meshHeading | pubmed-meshheading:17725607... | lld:pubmed |
| pubmed-article:17725607 | pubmed:meshHeading | pubmed-meshheading:17725607... | lld:pubmed |
| pubmed-article:17725607 | pubmed:meshHeading | pubmed-meshheading:17725607... | lld:pubmed |
