pubmed-article:19509224 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19509224 | lifeskim:mentions | umls-concept:C0014653 | lld:lifeskim |
pubmed-article:19509224 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
pubmed-article:19509224 | lifeskim:mentions | umls-concept:C0079731 | lld:lifeskim |
pubmed-article:19509224 | lifeskim:mentions | umls-concept:C0039198 | lld:lifeskim |
pubmed-article:19509224 | lifeskim:mentions | umls-concept:C2936411 | lld:lifeskim |
pubmed-article:19509224 | lifeskim:mentions | umls-concept:C0205282 | lld:lifeskim |
pubmed-article:19509224 | pubmed:issue | 13 | lld:pubmed |
pubmed-article:19509224 | pubmed:dateCreated | 2009-7-2 | lld:pubmed |
pubmed-article:19509224 | pubmed:abstractText | Using biopsy specimens from patients with B-cell non-Hodgkin's lymphoma, we observed a significantly low frequency of T(H)17 cells, including several samples with no detectable amount of interleukin (IL)-17-producing cells present in the tumor microenvironment. We found that, in the absence of lymphoma B cells, treatment with IL-1beta/IL-6 or lipopolysaccharide (LPS) enhanced IL-17 expression in CD4(+) T cells and this enhancement was attenuated when CD4(+) T cells were cocultured with lymphoma B cells. Blockade of CD27-CD70 or CD28-CD80/86 interactions by anti-CD70 or anti-CD80/86 antibodies restored LPS-mediated induction of IL-17 expression in CD4(+) T cells cocultured with lymphoma B cells. Because a subset of lymphoma B cells express IL-2 and given that IL-2 signaling is critically important in the development of regulatory T (T(reg)) cells, we tested the role of IL-2 signaling in T(H)17 cell development. We found that treatment with anti-IL-2 antibody to interrupt IL-2 signaling significantly inhibited Foxp3 expression in CD4(+) T cells. In contrast, interruption of IL-2 signaling up-regulated IL-17 expression in CD4(+) T cells and restored lymphoma-mediated down-regulation of IL-17-producing cells. Furthermore, the reversal of T(reg) cell activity by LPS or CpG-A resulted in an enhancement of IL-17-producing cells. Taken together, our study indicated that lymphoma B cells play an important role in skewing the balance between T(reg) and T(H)17 cells resulting in the establishment of a profoundly inhibitory tumor microenvironment. | lld:pubmed |
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pubmed-article:19509224 | pubmed:language | eng | lld:pubmed |
pubmed-article:19509224 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19509224 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:19509224 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19509224 | pubmed:month | Jul | lld:pubmed |
pubmed-article:19509224 | pubmed:issn | 1538-7445 | lld:pubmed |
pubmed-article:19509224 | pubmed:author | pubmed-author:AnsellStephen... | lld:pubmed |
pubmed-article:19509224 | pubmed:author | pubmed-author:WitzigThomas... | lld:pubmed |
pubmed-article:19509224 | pubmed:author | pubmed-author:NovakAnne JAJ | lld:pubmed |
pubmed-article:19509224 | pubmed:author | pubmed-author:YangZhi-Zhang... | lld:pubmed |
pubmed-article:19509224 | pubmed:author | pubmed-author:ZiesmerSteven... | lld:pubmed |
pubmed-article:19509224 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19509224 | pubmed:day | 1 | lld:pubmed |
pubmed-article:19509224 | pubmed:volume | 69 | lld:pubmed |
pubmed-article:19509224 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19509224 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19509224 | pubmed:pagination | 5522-30 | lld:pubmed |
pubmed-article:19509224 | pubmed:dateRevised | 2011-6-6 | lld:pubmed |
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