Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2001-4-6
pubmed:abstractText
We have previously shown that CD4(+) T cell-mediated allergic inflammation is diminished in signal transducer and activator of transcription (Stat)5a-deficient (Stat5a(-/-)) mice. To determine whether Stat5a regulates T helper cell differentiation, we studied T helper (Th)1 and Th2 cell differentiation of Stat5a(-/-)CD4(+) T cells at single-cell levels. First, Th2 cell differentiation from antigen-stimulated splenocytes was significantly decreased in Stat5a(-/-) mice as compared with that in wild-type mice. Further, Th2 cell differentiation was also impaired in Stat5a(-/-) mice even when purified CD4(+) T cells were stimulated with anti-CD3 plus anti-CD28 antibodies in the presence of interleukin-4. Moreover, the retrovirus-mediated gene expression of Stat5a in Stat5a(-/-)CD4(+) T cells restored the Th2 cell differentiation at the similar levels to that in wild-type CD4(+) T cells. In addition, interleukin-4 normally phosphorylated Stat6 in CD4(+) T cells from Stat5a(-/-) mice. Second, the development of CD4(+)CD25(+) immunoregulatory T cells was impaired in Stat5a(-/-) mice, as indicated by a significant decrease in the number of CD4(+)CD25(+) T cells in Stat5a(-/-) mice. Furthermore, the depletion of CD4(+)CD25(+) T cells from wild-type splenocytes significantly decreased Th2 cell differentiation but increased Th1 cell differentiation, whereas the depletion of CD4(+)CD25(+) T cells from Stat5a(-/-) splenocytes had no significant effect on the Th1 and Th2 cell differentiation. Together, these results indicate that the intrinsic expression of Stat5a in CD4(+) T cells is required for Th2 cell differentiation and that Stat5a is involved in the development of CD4(+)CD25(+) immunoregulatory T cells that modulate T helper cell differentiation toward Th2 cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4, http://linkedlifedata.com/resource/pubmed/chemical/Milk Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2, http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins, http://linkedlifedata.com/resource/pubmed/chemical/STAT5 Transcription Factor, http://linkedlifedata.com/resource/pubmed/chemical/STAT6 Transcription Factor, http://linkedlifedata.com/resource/pubmed/chemical/Stat5a protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Stat6 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2358-65
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11290598-Animals, pubmed-meshheading:11290598-Antigens, CD4, pubmed-meshheading:11290598-Cell Cycle, pubmed-meshheading:11290598-Cell Differentiation, pubmed-meshheading:11290598-DNA-Binding Proteins, pubmed-meshheading:11290598-Gene Expression, pubmed-meshheading:11290598-Interleukin-4, pubmed-meshheading:11290598-Mice, pubmed-meshheading:11290598-Mice, Inbred C57BL, pubmed-meshheading:11290598-Mice, Knockout, pubmed-meshheading:11290598-Mice, Transgenic, pubmed-meshheading:11290598-Milk Proteins, pubmed-meshheading:11290598-Receptors, Interleukin-2, pubmed-meshheading:11290598-Recombinant Fusion Proteins, pubmed-meshheading:11290598-STAT5 Transcription Factor, pubmed-meshheading:11290598-STAT6 Transcription Factor, pubmed-meshheading:11290598-Specific Pathogen-Free Organisms, pubmed-meshheading:11290598-Spleen, pubmed-meshheading:11290598-Th1 Cells, pubmed-meshheading:11290598-Th2 Cells, pubmed-meshheading:11290598-Trans-Activators
pubmed:year
2001
pubmed:articleTitle
Stat5a regulates T helper cell differentiation by several distinct mechanisms.
pubmed:affiliation
Department of Internal Medicine II, Chiba University School of Medicine, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't