Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-2-13
pubmed:abstractText
The T helper subsets Th1 and Th2 regulate specific types of immune responses by producing distinct sets of cytokines. Differentiation of the T helper subsets from their common precursors, naive CD4+ T cells, is induced by antigen stimulation and controlled by various other conditions. Of these conditions, the contributions of the cytokine environment have been the best characterized. The presence of interleukin-4 (IL-4) directs the differentiation towards Th2 cells, whereas IL-12 induces Thl differentiation. The Th2 signature cytokine genes encoding IL-4, IL-13, and IL-5 are clustered, and noncoding regions such as the intergenic region of the IL-4 and IL-13 genes are highly conserved from mice to humans. Alteration of the chromatin structure of this Th2 cytokine cluster region is detected as nuclease-accessible regions specific to Th2 cells. Activation of STAT6 promotes Th2 differentiation by inducing Th2-specific transcription factors, including GATA3. Expression of GATA3 induces Th2 differentiation and enhances the Th2 cell-specific chromatin accessibility, indicating that GATA3 is a key protein that regulates differentiation through chromatin remodeling. T helper subset differentiation provides a good system to study gene expression regulation at the chromatin level.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1521-6543
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
473-8
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Chromatin remodeling and T helper subset differentiation.
pubmed:affiliation
Department of Molecular and Developmental Biology, Institute of Medical Science, University of Tokyo, Japan.
pubmed:publicationType
Journal Article, Review