Dissection of the signalling mechanisms underlying FcgammaRIIB-mediated apoptosis of mature B-cells.
The low-affinity receptor for IgG, FcgammaRIIB, 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 FcgammaRIIB results in growth arrest and apoptosis. We have now investigated the signals underlying FcgammaRIIB-driven apoptosis and found this to be dependent on disruption of mitochondrial potential (Deltapsi), involve the pro-apoptotic Bcl-2 family members, Bid and Bad, and be caspase-independent.
Carter
N A
NA
Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow G11 6NT, UK. 0105567c@student.gla.ac.uk
Harnett
M M
MM
D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D001402:B-Lymphocytes / Q000276:immunology*; D061945:Caspase Inhibitors; D002478:Cells, Cultured; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D008213:Lymphocyte Activation; D008564:Membrane Potentials; D008928:Mitochondria / Q000276:immunology / Q000502:physiology; D011947:Receptors, Antigen, B-Cell / Q000276:immunology; D017452:Receptors, IgG / Q000502:physiology*; D015398:Signal Transduction / Q000276:immunology*
D061945:Caspase Inhibitors; D004791:Enzyme Inhibitors; C445323:FCGR2A protein, human; C499173:FCGR2B protein, human; D011947:Receptors, Antigen, B-Cell; D017452:Receptors, IgG