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 () and Ji-Yang Wang ()
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Yingqian Li: School of Basic Medical Sciences, Fudan University
Yoshimasa Takahashi: National Institute of Infectious Diseases
Shin-ichiro Fujii: Laboratory for Immunotherapy, Center for Integrative Medical Sciences, RIKEN
Yang Zhou: School of Basic Medical Sciences, Fudan University
Rongjian Hong: School of Basic Medical Sciences, Fudan University
Akari Suzuki: Laboratory for Autoimmune Diseases, Center for Integrative Medical Sciences, RIKEN
Takeshi Tsubata: Medical Research Institute, Tokyo Medical and Dental University
Koji Hase: International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo
Ji-Yang Wang: School of Basic Medical Sciences, Fudan University

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract 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.

Date: 2016
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DOI: 10.1038/ncomms10836

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