| Abstract |
This thesis describes the FcγR expression of macrophages and which of these receptors contribute to the phagocytosis of IgG-opsonized particles. By using a model of IgGopsonized erythrocyte clearance by in vitro cultured macrophages, we studied how intravenous immunoglobulin (IVIG), which is used in the treatment of a variety of immune diseases, may prevent the phagocytosis of autoantibody-opsonized blood cells by these macrophages. Moreover, we studied the underlying mechanisms regarding IgG-mediated extravascular hemolysis, a severe side effect of IVIG treatment.
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