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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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B cell apoptosis triggered by antigen receptor ligation proceeds via a novel caspase-dependent pathway.

In contrast to positive signaling leading to proliferation, the mechanisms involved in negative signaling culminating in apoptosis after B cell Ag receptor (BCR) ligation have received little study. We find that apoptosis induced by BCR cross-linking on EBV-negative mature and immature human B cell lines involves the following sequential, required events: a cyclosporin A-inhibitable, likely calcineurin-mediated step; and activation of caspase-2, -3, and -9. Caspase-2 is activated early and plays a major role in the apoptotic pathway, while caspase-9 is activated later in the apoptotic pathway and most likely functions to amplify the apoptotic signal. Caspase-8 and -1, which are activated by ligation of the CD95 and TNF-R1 death receptors, are not involved. Apoptosis induced by BCR ligation thus proceeds via a previously unreported intracellular signaling pathway.[1]

References

  1. B cell apoptosis triggered by antigen receptor ligation proceeds via a novel caspase-dependent pathway. Chen, W., Wang, H.G., Srinivasula, S.M., Alnemri, E.S., Cooper, N.R. J. Immunol. (1999) [Pubmed]
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