Linked Life Data

17137775

Source:http://linkedlifedata.com/resource/pubmed/id/17137775

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-1-15
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0952-7915
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
55-62
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Transforming growth factor-beta: innately bipolar.
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
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Intramural