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• W3017756171 abstract "The adaptor protein, STING (stimulator of interferon genes), has been rarely studied in adaptive immunity. We used Sting KO mice and a patient's mutated STING cells to study the effect of STING deficiency on B cell development, differentiation, and BCR signaling. We found that STING deficiency promotes the differentiation of marginal zone B cells. STING is involved in BCR activation and negatively regulates the activation of CD19 and Btk but positively regulates the activation of SHIP. The activation of WASP and accumulation of F-actin were enhanced in Sting KO B cells upon BCR stimulation. Mechanistically, STING uses PI3K mediated by the CD19-Btk axis as a central hub for controlling the actin remodeling that, in turn, offers feedback to BCR signaling. Overall, our study provides a mechanism of how STING regulates BCR signaling via feedback from actin reorganization, which contributes to positive regulation of STING on the humoral immune response." @default.
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• W3017756171 date "2020-04-24" @default.
• W3017756171 modified "2023-10-05" @default.
• W3017756171 title "STING couples with PI3K to regulate actin reorganization during BCR activation" @default.
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• W3017756171 doi "https://doi.org/10.1126/sciadv.aax9455" @default.
• W3017756171 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7176427" @default.
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