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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