| pubmed-article:17137775 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17137775 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
| pubmed-article:17137775 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:17137775 | pubmed:dateCreated | 2007-1-15 | lld:pubmed |
| pubmed-article:17137775 | pubmed:abstractText | Widely heralded for depressing ongoing immune responses, renewed interest in the proficiency by which transforming growth factor beta (TGF-beta) not only engages but also might drive an over-reactive innate response highlights its bipolar nature. Although coordination of the development and function of Treg, in addition to direct inhibition of cellular activation, are prominent pathways by which TGF-beta controls adaptive immunity, paradoxically TGF-beta appears instrumental in initiation of host responses to invasion through recruitment and activation of immune cells and persuasion of Th17 lineage commitment. Nevertheless, true to its manic-depressive behavior, new evidence links TGF-beta with depression of innate cells, including NK cells, and by way of a potential bridge between mast cells and Treg. Disruption of the tenuous balance between these opposing actions of TGF-beta underlies immunopathogenicity. | lld:pubmed |
| pubmed-article:17137775 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17137775 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17137775 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17137775 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17137775 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17137775 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:17137775 | pubmed:issn | 0952-7915 | lld:pubmed |
| pubmed-article:17137775 | pubmed:author | pubmed-author:WahlSharon... | lld:pubmed |
| pubmed-article:17137775 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17137775 | pubmed:volume | 19 | lld:pubmed |
| pubmed-article:17137775 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17137775 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17137775 | pubmed:pagination | 55-62 | lld:pubmed |
| pubmed-article:17137775 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
| pubmed-article:17137775 | pubmed:meshHeading | pubmed-meshheading:17137775... | lld:pubmed |
| pubmed-article:17137775 | pubmed:meshHeading | pubmed-meshheading:17137775... | lld:pubmed |
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| pubmed-article:17137775 | pubmed:meshHeading | pubmed-meshheading:17137775... | lld:pubmed |
| pubmed-article:17137775 | pubmed:meshHeading | pubmed-meshheading:17137775... | lld:pubmed |
| pubmed-article:17137775 | pubmed:meshHeading | pubmed-meshheading:17137775... | lld:pubmed |
| pubmed-article:17137775 | pubmed:meshHeading | pubmed-meshheading:17137775... | lld:pubmed |
| pubmed-article:17137775 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17137775 | pubmed:articleTitle | Transforming growth factor-beta: innately bipolar. | lld:pubmed |
| pubmed-article:17137775 | pubmed:affiliation | Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH), Bethesda, MD 20892-4352, USA. smwahl@dir.nidcr.nih.gov | lld:pubmed |
| pubmed-article:17137775 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17137775 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:17137775 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
| entrez-gene:7040 | entrezgene:pubmed | pubmed-article:17137775 | lld:entrezgene |
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