Linked Life Data

11745386

Source:http://linkedlifedata.com/resource/pubmed/id/11745386

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2001-12-17
pubmed:abstractText
Transforming growth factor-beta1 (TGF-beta1) is an inhibitory cytokine increasingly recognized as a key factor for immuno-regulation. The function of IL-4 in the regulation of TGF-beta1 production from T cells has been reported previously; however, the precise molecular mechanism still remains to be elucidated. For a better understanding of the mechanism involved in regulation, we have investigated a relationship between the STAT6-dependent pathway and TGF-beta1 production from naïve T cells. TCR crosslinking initiates TGF-beta1 production in CD4(+) T cells, and IL-4-mediated signaling enhances the TGF-beta1 production from naïve CD4(+) T cells. The IL-4-mediated up-regulation of TGF-beta1 production from naïve CD4(+) T cells is elicited in STAT6-deficient (STAT6 KO) mice, but not in IL-4 receptor-deficient (IL-4R KO) mice. These results clearly demonstrate that a STAT6-independent pathway is working in IL-4-mediated enhancement of TGF-beta1 production from naïve CD4(+) T cells. Moreover, the addition of IL-4 showed no additive effect on TGF-beta1 promoter-mediated transcription stimulated by TCR. Therefore, we hypothesize that the IL-4-mediated signaling does not work directly on the transcription of the TGF-beta1 gene, but rather regulates the expansion of TGF-beta1-secreting T cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3659-66
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
IL-4-mediated development of TGF-beta1-producing cells from naïve CD4(+) T cells through a STAT6-independent mechanism.
pubmed:affiliation
Research Institute for Biological Sciences, Science University of Tokyo, Chiba, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't