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• W2975942999 abstract "Abstract The pathway of homeostatic IgG extravasation is not fully understood, in spite of its importance for the maintenance of host immunity, the management of autoantibody-mediated disorders, and the use of antibody-based biologics. Here we show in a murine model of pemphigus, a prototypic cutaneous autoantibody-mediated disorder, that blood-circulating IgG extravasates into the skin in a time- and dose-dependent manner under homeostatic conditions. This IgG extravasation is unaffected by depletion of Fcγ receptors, but is largely attenuated by specific ablation of dynamin-dependent endocytic vesicle formation in blood endothelial cells (BECs). Among dynamin-dependent endocytic vesicles, IgG co-localizes well with caveolae in cultured BECs. An Abl family tyrosine kinase inhibitor imatinib, which reduces caveolae-mediated endocytosis, impairs IgG extravasation in the skin and attenuates the murine pemphigus manifestations. Our study highlights the kinetics of IgG extravasation in vivo, which might be a clue to understand the pathological mechanism of autoantibody-mediated autoimmune disorders." @default.
• W2975942999 created "2019-10-03" @default.
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• W2975942999 date "2019-09-30" @default.
• W2975942999 modified "2023-10-16" @default.
• W2975942999 title "Abl family tyrosine kinases govern IgG extravasation in the skin in a murine pemphigus model" @default.
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• W2975942999 doi "https://doi.org/10.1038/s41467-019-12232-3" @default.
• W2975942999 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6769004" @default.
• W2975942999 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31570755" @default.
• W2975942999 hasPublicationYear "2019" @default.
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