Abstract

Current treatment strategies in patients with immunothrombocytopenia (ITP) include immunosuppression and the stimulation of platelet production. Research over the last decade has emphasized the important role of Fc-receptors as key molecules responsible for autoantibody-mediated platelet depletion, allowing for a more specific targeting of this pathway instead of a generalized suppression of the immune system. This short review will discuss approaches aiming at interfering with key steps in this pathway, such as preventing the interaction of the platelet autoantibody immune complex with phagocytic cells, enhancing the clearance of autoantibodies, and interfering with or modulating the signaling pathways responsible for innate immune effector cell activation.

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