CD40
下调和上调
CD19
幼稚B细胞
B细胞
B细胞激活因子
免疫系统
免疫学
生物
T细胞
医学
抗原提呈细胞
细胞毒性T细胞
体外
抗体
基因
生物化学
作者
Mingen Lyu,Yushu Hao,Yang Li,Cuicui Lyu,Wenjie Liu,Huiyuan Li,Feng Xue,Xiaofan Liu,Renchi Yang
摘要
CD72 is a co-receptor of B cells and regulates B cell activation. Although aberrant expression of CD72 has been reported in primary immune thrombocytopenia (ITP), it is uncertain whether this aberrant expression is restricted to specific B cell subsets. Furthermore, the mechanisms that regulate CD72 expression are unknown. In this study, we found higher frequency of CD19+ B cells, CD19+ CD27+ memory B cells and lower frequency of CD19+ CD27- naive B cells in active ITP patients compared with controls and patients in remission. CD72 expression on CD19+ CD27+ cells was upregulated in active ITP patients and correlated with platelet count and anti-platelet autoantibodies. In vitro, CD40L could specifically induce CD72 upregulation on CD19+ CD27+ B cells. In combination with CD40L, interleukin (IL) 10 and BAFF (also termed TNFSF13B) further enhanced CD72 expression on CD19+ CD27+ B cells, whereas IL21 reduced CD72 upregulation. CD72mRNA expression after CD40L stimulation was increased in ITP patients and controls. Significant increase of CD40L on CD4+ T cells was correlated with CD72 expression on CD19+ CD27+ B cells in ITP patients. In conclusion, upregulation of CD72 expression on CD27+ memory B cells might take part in the pathogenesis of ITP. Elevated CD40L on CD4+ cells combined with cytokines might contribute to the upregulation of CD72 expression on CD27+ memory B cells.
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