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The mononuclear phagocyte system (MPS) receptors and serum opsonins constitute a critical biological clearance mechanism and immune defense system. Serum opsonins, such as antibodies (IgG) and complement proteins (C3b), coat foreign particles, pathogens, or damaged cells to facilitate their recognition. These opsonized entities are then bound by specific receptors on the surface of mononuclear phagocytes—including monocytes, macrophages, and dendritic cells—such as Fc receptors and complement receptors. This interaction triggers phagocytosis, leading to the internalization and degradation of the target. While essential for immunity and homeostasis, the MPS also acts as a major barrier to the delivery of therapeutic nanoparticles and liposomes, which are often rapidly cleared from circulation by these cells. Modulating this system is a key strategy in drug delivery, such as through PEGylation to avoid clearance, or in treating conditions like autoimmune diseases and lysosomal storage disorders by targeting specific macrophage receptors. Understanding the interplay between opsonins and MPS receptors is crucial for optimizing drug half-life and minimizing off-target immune activation.
Opsonization of targets by serum proteins (e.g., IgG, C3b) followed by receptor-mediated phagocytosis (e.g., via FcR, CR) by mononuclear phagocytes.
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