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- W1514581105 abstract "Abstract The plasma membrane of B cells is at risk for injury by bacterial toxins, viruses, and possible mechanical damage induced by interactions with other cells during antigen presentation. Whether and how B cells repair membrane damage and its impact on B-cell functions are unknown. Here we show that upon injury by the pore forming toxin streptolysin O (SLO), primary mouse splenic B cells can repair their membrane in a Ca2+-dependent manner, like muscle and epithelial cells. B cells exocytose their lysosomes in response to Ca2+ influx and release acid sphingomyelinase from lysosomes, which induces endocytosis. In B cells activated by cross-linking B-cell receptors (BCRs), repairing membrane damage by SLO inhibits BCR clustering and internalization, consequently reducing BCR-induced tyrosine phosphorylation. Further analyses show that membrane repair inhibits the colocalization of BCRs with lipid rafts on the cell surface and during their internalization, indicating that membrane repair-induced endocytosis competes with BCRs for lipid rafts and interferes with the interaction of BCRs with lipid raft-associated kinases. Our results reveal the ability and the mechanism for B cells to repair membrane damage, and discover a negative regulatory role of membrane repair on B cell signaling and antigen uptake functions." @default.
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- W1514581105 date "2014-05-01" @default.
- W1514581105 modified "2023-09-28" @default.
- W1514581105 title "Mechanism of B cell membrane repair and the effects of repair on B cell receptor activation (IRC3P.460)" @default.
- W1514581105 doi "https://doi.org/10.4049/jimmunol.192.supp.59.3" @default.
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