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

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  • Yingqian Li

    (School of Basic Medical Sciences, Fudan University
    International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo
    Faculty of Pharmacy, Keio 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
    Faculty of Pharmacy, Keio University)

  • Ji-Yang Wang

    (School of Basic Medical Sciences, Fudan University
    Medical Research Institute, Tokyo Medical and Dental University)

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.

Suggested Citation

  • Yingqian Li & Yoshimasa Takahashi & Shin-ichiro Fujii & Yang Zhou & Rongjian Hong & Akari Suzuki & Takeshi Tsubata & Koji Hase & Ji-Yang Wang, 2016. "EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity," Nature Communications, Nature, vol. 7(1), pages 1-13, April.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10836
    DOI: 10.1038/ncomms10836
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    Cited by:

    1. Sophie Hillion & Anjelica Miranda & Christelle Dantec & Marina Boudigou & Laëtitia Pottier & Divi Cornec & Raul M. Torres & Roberta Pelanda, 2024. "Maf expression in B cells restricts reactive plasmablast and germinal center B cell expansion," Nature Communications, Nature, vol. 15(1), pages 1-16, December.

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