rdf:type |
|
lifeskim:mentions |
umls-concept:C0021081,
umls-concept:C0037083,
umls-concept:C0039194,
umls-concept:C0040690,
umls-concept:C0152060,
umls-concept:C0205154,
umls-concept:C0220905,
umls-concept:C1306235,
umls-concept:C1332714,
umls-concept:C1334114,
umls-concept:C1514873,
umls-concept:C1515655,
umls-concept:C1516240,
umls-concept:C1546857,
umls-concept:C1556066,
umls-concept:C1619636,
umls-concept:C1710082
|
pubmed:issue |
11
|
pubmed:dateCreated |
2004-11-23
|
pubmed:abstractText |
Data regarding the role of TGF-beta for the in vivo function of regulatory CD4(+)CD25(+) T cells (Treg) are controversial. A transgenic mouse model with impaired TGF-beta signaling specifically in T cells was used to assess the role of endogenous TGF-beta for the in vivo function of CD4(+)CD25(+) Treg in a murine model of colitis induced by dextran sulfate. Transfer of wild-type, but not transgenic CD4(+)CD25(+) Treg was found to suppress colitis in wild-type mice. In addition, by transferring CFSE-labeled CD4(+)CD25(+) Treg we could demonstrate that endogenous TGF-beta promotes the expansion of CD4(+)CD25(+) Treg in vivo. Transgenic mice themselves developed reduced numbers of peripheral CD4(+)CD25(+) Treg and were more susceptible to the induction of colitis, which could be prevented by the transfer of wild-type Treg. These data indicate that TGF-beta signaling in CD4(+)CD25(+) Treg is required for their in vivo expansion and suppressive capacity.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0022-1767
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
1
|
pubmed:volume |
173
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
6526-31
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:15557141-Adoptive Transfer,
pubmed-meshheading:15557141-Animals,
pubmed-meshheading:15557141-Cell Differentiation,
pubmed-meshheading:15557141-Colitis,
pubmed-meshheading:15557141-Genetic Predisposition to Disease,
pubmed-meshheading:15557141-Humans,
pubmed-meshheading:15557141-Lymphocyte Count,
pubmed-meshheading:15557141-Mice,
pubmed-meshheading:15557141-Receptors, Interleukin-2,
pubmed-meshheading:15557141-Signal Transduction,
pubmed-meshheading:15557141-T-Lymphocytes, Regulatory,
pubmed-meshheading:15557141-Transforming Growth Factor beta
|
pubmed:year |
2004
|
pubmed:articleTitle |
Cutting edge: TGF-beta signaling is required for the in vivo expansion and immunosuppressive capacity of regulatory CD4+CD25+ T cells.
|
pubmed:affiliation |
I. Medizinische Klinik, Johannes Gutenberg-Universität, Mainz, Germany.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|