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STING couples with PI3K to regulate actin reorganization during BCR activation

Jiang PP; Miller H; Yang L; Mattila PK; Ning Q; Liu Z; Kang DQ; Cheng JL; Yin W; Li N; Yu B; Sun JQ; Ren BX; Liu CH; Dai X; Jing YK; Gong Q; Li JW

dc.contributor.authorJiang PP
dc.contributor.authorMiller H
dc.contributor.authorYang L
dc.contributor.authorMattila PK
dc.contributor.authorNing Q
dc.contributor.authorLiu Z
dc.contributor.authorKang DQ
dc.contributor.authorCheng JL
dc.contributor.authorYin W
dc.contributor.authorLi N
dc.contributor.authorYu B
dc.contributor.authorSun JQ
dc.contributor.authorRen BX
dc.contributor.authorLiu CH
dc.contributor.authorDai X
dc.contributor.authorJing YK
dc.contributor.authorGong Q
dc.contributor.authorLi JW
dc.date.accessioned2022-10-28T13:54:00Z
dc.date.available2022-10-28T13:54:00Z
dc.identifier.urihttps://www.utupub.fi/handle/10024/168145
dc.description.abstractThe 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.
dc.language.isoen
dc.publisherAMER ASSOC ADVANCEMENT SCIENCE
dc.titleSTING couples with PI3K to regulate actin reorganization during BCR activation
dc.identifier.urnURN:NBN:fi-fe2021042824161
dc.relation.volume6
dc.contributor.organizationfi=biolääketieteen laitos, yhteiset|en=Institute of Biomedicine|
dc.contributor.organizationfi=MediCity|en=MediCity Research Laboratory|
dc.contributor.organization-code2607100
dc.converis.publication-id47734182
dc.converis.urlhttps://research.utu.fi/converis/portal/Publication/47734182
dc.identifier.eissn2375-2548
dc.identifier.jour-issn2375-2548
dc.okm.affiliatedauthorMattila, Pieta
dc.okm.affiliatedauthorDataimport, MediCity
dc.okm.discipline3111 Biomedicineen_GB
dc.okm.discipline3111 Biolääketieteetfi_FI
dc.okm.internationalcopublicationinternational co-publication
dc.okm.internationalityInternational publication
dc.okm.typeJournal article
dc.publisher.countryUnited Statesen_GB
dc.publisher.countryYhdysvallat (USA)fi_FI
dc.publisher.country-codeUS
dc.relation.articlenumberARTN eaax9455
dc.relation.doi10.1126/sciadv.aax9455
dc.relation.ispartofjournalScience Advances
dc.relation.issue17
dc.year.issued2020


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