A1 Refereed original research article in a scientific journal
STING couples with PI3K to regulate actin reorganization during BCR activation
Authors: Jing YK, Dai X, Yang L, Kang DQ, Jiang PP, Li N, Cheng JL, Li JW, Miller H, Ren BX, Gong Q, Yin W, Liu Z, Mattila PK, Ning Q, Sun JQ, Yu B, Liu CH
Publisher: AMER ASSOC ADVANCEMENT SCIENCE
Publication year: 2020
Journal: Science Advances
Journal name in source: SCIENCE ADVANCES
Journal acronym: SCI ADV
Article number: ARTN eaax9455
Volume: 6
Issue: 17
Number of pages: 14
ISSN: 2375-2548
eISSN: 2375-2548
DOI: https://doi.org/10.1126/sciadv.aax9455(external)
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/47734182(external)
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 CD1 9 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.
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