L’antagoniste se lie à Blys

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Presentation transcript:

L’antagoniste se lie à Blys Les antagonistes de Blys favorisent l’apoptose des lymphocytes B autoréactifs Maladie auto-immune L’antagoniste se lie à Blys Le lymphocyte B survit Excess BLyS promotes the survival of autoreactive B cells otherwise destined for apoptosis; BLys antagonists allow apoptosis to proceed. BLyS antagonists block BLyS from binding to its receptor; such blocking prevents NF-B signaling and upregulation of anti-apoptotic genes. Without these “survival” proteins, the B cell undergoes apoptosis.1,2 Because BLyS receptors are not expressed at every stage of B-cell development, BLyS-targeted therapy is restricted to early-stage B cells in the periphery without affecting late-stage compartments, such as memory or bone marrow plasma cells, and without compromising immunity.3 By reducing BLyS levels to “normal” or below a threshold critical for an autoimmune response, antagonists may potentially ameliorate SLE.4 References Kanakaraj P et al. BLyS binds to B cells with high affinity and induces activation of the transcription factors Nf-kappa-β and ELF-1. Cytokine. 2001;13:25-31. Do RK et al. Attenuation of apoptosis underlies B lymphocyte stimulator enhancement of humoral immune response. J Exp Med. 2000;192:953-64. Cancro MP et al. The role of B lymphocyte stimulator (BLyS) in systemic lupus erythematosus. J Clin Invest. 2009;119:1066-73. Stohl W. BlySfulness does not equal blissfulness in systemic lupus erythematosus: a therapeutic role for BLyS antagonists. Curr Dir Autoimmun. 2005;8:289-304. Le lymphocyte B meurt BLyS BR3 or TACI or BCMA Antagoniste de Blys 1 Cancro MP et al. J Clin Invest. 2009;119:1066-73.