EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity

Yingqian Li, Yoshimasa Takahashi, Shin Ichiro Fujii, Yang Zhou, Rongjian Hong, Akari Suzuki, Takeshi Tsubata, Koji Hase, Ji Yang Wang

研究成果: Article査読

16 被引用数 (Scopus)

抄録

Regulated apoptosis of germinal centre (GC) B cells is critical for normal humoral immune responses. ELL-associated factor 2 (EAF2) regulates transcription elongation and has been shown to be an androgen-responsive potential tumour suppressor in prostate by inducing apoptosis. Here we show that EAF2 is selectively upregulated in GC B cells among various immune cell types and promotes apoptosis of GC B cells both in vitro and in vivo. EAF2 deficiency results in enlarged GCs and elevated antibody production during a T-dependent immune response. After immunization with type II collagen, mice lacking EAF2 produce high levels of collagen-specific autoantibodies and rapidly develop severe arthritis. Moreover, the mutant mice spontaneously produce anti-dsDNA, rheumatoid factor and anti-nuclear antibodies as they age. These results demonstrate that EAF2-mediated apoptosis in GC B cells limits excessive humoral immune responses and is important for maintaining self-tolerance.

本文言語English
論文番号10836
ジャーナルNature communications
7
DOI
出版ステータスPublished - 2016 3月 3

ASJC Scopus subject areas

  • 化学 (全般)
  • 生化学、遺伝学、分子生物学(全般)
  • 物理学および天文学(全般)

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