The low-affinity receptor for IgG, FcγRIIB, negatively regulates BCR (B-cell antigen receptor)-mediated proliferative signalling and thus plays an important role in feedback inhibition of the humoral immune response. Whereas crosslinking of BCR on mature B-cells results in proliferation, co-ligation of FcγRIIB results in growth arrest and apoptosis. We have now investigated the signals underlying FcγRIIB-driven apoptosis and found this to be dependent on disruption of mitochondrial potential (Δψ), involve the pro-apoptotic Bcl-2 family members, Bid and Bad, and be caspase-independent.
Conference Article| October 26 2004
Dissection of the signalling mechanisms underlying FcγRIIB-mediated apoptosis of mature B-cells
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N.A. Carter, M.M. Harnett; Dissection of the signalling mechanisms underlying FcγRIIB-mediated apoptosis of mature B-cells. Biochem Soc Trans 1 November 2004; 32 (6): 973–975. doi: https://doi.org/10.1042/BST0320973
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