Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2008-8-4
pubmed:abstractText
Our previous studies have shown that Foxp3 under the control of IFN-gamma promoter (IgammaP-Foxp3) converts pathogenic CD4(+)Th1 cells into regulatory T cells (Tregs), which control diabetes in non-obese diabetic (NOD) mice. Here, we tested the other hypothesis that transient expression of Foxp3 as controlled by the transient expression of IL-12Rbeta2 during Th1 cell derivation is sufficient to convert cells to Tregs. Foxp3, under the control of IL-12Rbeta2 promoter (Ibeta2P), was lentivirally transduced into naïve CD4(+)T cells from NOD mice. Ibeta2P-Foxp3-transduced CD4(+)T cells could not effectively suppress the incidence of diabetes when transferred into NOD mice. Furthermore, we found that Ibeta2P-Foxp3-transduced CD4(+)T cells, stimulated by a high dose of autoantigen, did not suppress CD4(+)T cell activation, produce CD4(+)Foxp3(+)Tregs, and up-regulate CTLA4 expression. These results suggest that Ibeta2P cannot mediate Foxp3 to convert pathogenic CD4(+)Th1 cells into Tregs which control diabetes in NOD mice.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0161-5890
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3814-7
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Diabetes is not prevented by Foxp3-transduced CD4(+)T cells under the IL-12Rbeta2 promoter control.
pubmed:affiliation
Department of Molecular Immunology, Institute of Basic Medical Sciences, Taiping Road, No. 27, Beijing 100850, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't