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10.1038/ncomms10836

http://scihub22266oqcxt.onion/10.1038/ncomms10836
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C4782062!4782062!26935903
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suck abstract from ncbi


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pmid26935903      Nat+Commun 2016 ; 7 (ä): ä
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  • EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity #MMPMID26935903
  • Li Y; Takahashi Y; Fujii Si; Zhou Y; Hong R; Suzuki A; Tsubata T; Hase K; Wang JY
  • Nat Commun 2016[]; 7 (ä): ä PMID26935903show ga
  • 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.
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