The enhancer HS2 critically regulates GATA-3-mediated Il4 transcription in TH 2 cells

Shinya Tanaka, Yasutaka Motomura, Yoshie Suzuki, Ryoji Yagi, Hiromasa Inoue, Shoichiro Miyatake, Masato Kubo

研究成果: ジャーナルへの寄稿学術誌査読

93 被引用数 (Scopus)

抄録

GATA-3 is a master regulator of T helper type 2 (TH2) differentiation. However, the molecular basis of GATA-3-mediated TH 2 lineage commitment is poorly understood. Here we identify the DNase I-hypersensitive site 2 (HS2) element located in the second intron of the interleukin 4 locus (Il4) as a critical enhancer strictly controlled by GATA-3 binding. Mice lacking HS2 showed substantial impairment in their asthmatic responses and their production of IL-4 but not of other TH 2 cytokines. Overexpression of Gata3 in HS2-deficient T cells failed to restore Il4 expression. HS2 deletion impaired the trimethylation of histone H3 at Lys4 and acetylation of histone H3 at Lys9 and Lys14 in the Il4 locus. Our results indicate that HS2 is the target of GATA-3 in regulating chromosomal modification of the Il4 locus and is independent of the Il5 and Il13 loci.

本文言語英語
ページ(範囲)77-85
ページ数9
ジャーナルNature Immunology
12
1
DOI
出版ステータス出版済み - 1月 2011
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 免疫アレルギー学
  • 免疫学

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