This study investigates how various antagonists targeting the neonatal Fc receptor (FcRn) affect the intracellular trafficking and fate of FcRn and its ligand, albumin. The research aims to elucidate the mechanisms by which FcRn antagonists modulate albumin homeostasis, providing insights for therapeutic strategies that involve FcRn inhibition.
The findings reveal that different FcRn antagonists have distinct effects on the subcellular trafficking pathways of FcRn and albumin. Some antagonists promote the lysosomal degradation of albumin, while others enhance its recycling to the cell surface. These differential effects have significant implications for the design and therapeutic application of FcRn inhibitors.
The study utilized a humanized mouse model developed in collaboration with genOway. This model expresses the human FcRn receptor, allowing for the evaluation of human-specific FcRn-antagonist interactions and their impact on albumin dynamics in a physiological context.
Autoimmune diseases, Therapeutic antibodies, Protein homeostasis, Pharmacokinetics, FcRn-targeted therapy
Humanized FcRn expression, Transgenic mouse model, In vivo trafficking analysis, Receptor-ligand interaction, Therapeutic modulation
From model design to experimental results
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Models with certified health status from professional breeders in US and Europe
