摘要
The susceptibility of primary B cells to Fas (APO-1, CD95)-mediated apoptosis is regulated by signals derived from additional surface receptors. CD40 engagement produces upregulation of Fas expression and induces marked sensitivity to Fas-induced cell death, whereas B cell antigen receptor (BCR) engagement inhibits Fas killing and thereby produces Fas-resistance, even in otherwise susceptible, CD40-stimulated targets. BCR signaling for inducible Fas-resistance develops over a period of 12 hours and depends
