Abstract
Antibodies carry out effector functions either directly or by binding of immune complexes to cellular Fc-receptors. Here we focussed on two mouse models: a model for immune-thrombocytopenia, where platelets are depleted by injection of anti-platelet antibodies, and a model for lymphoma treatment, where B-cells are depleted by CD20-specific antibodies. In both cases we found the activating Fc-receptors FcγRI and IV to be essential for IgG activity.
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