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• W4366241066 endingPage "e0284636" @default.
• W4366241066 startingPage "e0284636" @default.
• W4366241066 abstract "Podocytes are key to preventing the filtration of serum proteins into the urine. Recent evidence also suggests that in immune mediated kidney diseases, podocytes are the targets of immune complexes (ICs). The mechanisms whereby podocytes handle and respond to ICs remain unknown. The neonatal Fc receptor (FcRn) is involved in IgG handling in podocytes and is also required in dendritic cells to traffic ICs to the lysosome for proteolytic degradation of antigen and presentation on MHC II. Here we examine the role of FcRn in handling ICs in podocytes. We show that knockout of FcRn in podocytes results in decreased trafficking of ICs to the lysosome and increases IC trafficking to recycling endosomes. FcRn KO also alters lysosomal distribution, decreases lysosomal surface area and decreases cathepsin B expression and activity. We demonstrate that signaling pathways in cultured podocytes differ after treatment with IgG alone versus ICs and that podocyte proliferation in both WT and KO podocytes is suppressed by IC treatment. Our findings suggest that podocytes respond differentially to IgG versus ICs and that FcRn modifies the lysosomal response to ICs. Elucidating the mechanisms underlying podocyte handling of ICs may provide novel pathways to modulate immune mediated kidney disease progression." @default.
• W4366241066 created "2023-04-20" @default.
• W4366241066 creator A5052100452 @default.
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• W4366241066 date "2023-04-18" @default.
• W4366241066 modified "2023-09-30" @default.
• W4366241066 title "Knockout of the neonatal Fc receptor alters immune complex trafficking and lysosomal function in cultured podocytes" @default.
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• W4366241066 doi "https://doi.org/10.1371/journal.pone.0284636" @default.
• W4366241066 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37071647" @default.
• W4366241066 hasPublicationYear "2023" @default.
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