Yan Feng

Publications (2)52.02 Total impact

• Source

  Available from: sibcb.ac.cn

  Article: Critical regulation of CD4+ T cell survival and autoimmunity by beta-arrestin 1.

  Yufeng Shi, Yan Feng, Jiuhong Kang, Chang Liu, Zhenxin Li, Dangsheng Li, Wei Cao, Ju Qiu, Zhengliang Guo, Enguang Bi, Lei Zang, Chuanzhen Lu, Jingwu Z Zhang, Gang Pei
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  ABSTRACT: CD4+ T cells are important in adaptive immunity, but their dysregulation can cause autoimmunity. Here we demonstrate that the multifunctional adaptor protein beta-arrestin 1 positively regulated naive and activated CD4+ T cell survival. We found enhanced expression of the proto-oncogene Bcl2 through beta-arrestin 1-dependent regulation of acetylation of histone H4 at the Bcl2 promoter. Mice deficient in the gene encoding beta-arrestin 1 (Arrb1) were much more resistant to experimental autoimmune encephalomyelitis, whereas overexpression of Arrb1 increased susceptibility to this disease. CD4+ T cells from patients with multiple sclerosis had much higher Arrb1 expression, and 'knockdown' of Arrb1 by RNA-mediated interference in those cells increased apoptosis induced by cytokine withdrawal. Our data demonstrate that beta-arrestin 1 is critical for CD4+ T cell survival and is a factor in susceptibility to autoimmunity.
  Nature Immunology 09/2007; 8(8):817-24. · 26.01 Impact Factor
• Article: Critical regulation of CD4+ T cell survival and autoimmunity by -arrestin 1

  Yufeng Shi, Yan Feng, Jiuhong Kang, Chang Liu, Zhenxin Li, Dangsheng Li, Wei Cao, Ju Qiu, Zhengliang Guo, Enguang Bi, Lei Zang, Chuanzhen Lu, Jingwu Z Zhang, Gang Pei
  [show abstract] [hide abstract]
  ABSTRACT: CD4+ T cells are important in adaptive immunity, but their dysregulation can cause autoimmunity. Here we demonstrate that the multifunctional adaptor protein -arrestin 1 positively regulated naive and activated CD4+ T cell survival. We found enhanced expression of the proto-oncogene Bcl2 through -arrestin 1–dependent regulation of acetylation of histone H4 at the Bcl2 promoter. Mice deficient in the gene encoding -arrestin 1 (Arrb1) were much more resistant to experimental autoimmune encephalomyelitis, whereas overexpression of Arrb1 increased susceptibility to this disease. CD4+ T cells from patients with multiple sclerosis had much higher Arrb1 expression, and 'knockdown' of Arrb1 by RNA-mediated interference in those cells increased apoptosis induced by cytokine withdrawal. Our data demonstrate that -arrestin 1 is critical for CD4+ T cell survival and is a factor in susceptibility to autoimmunity.
  Nature Immunology 07/2007; 8(8):817-824. · 26.01 Impact Factor