Matches in SemOpenAlex for { <https://semopenalex.org/work/W2767226775> ?p ?o ?g. }
- W2767226775 abstract "Mechanistic target of rapamycin (mTOR) enhances immunity in addition to orchestrating metabolism. Here we show that mTOR coordinates immunometabolic reconfiguration of marginal zone (MZ) B cells, a pre-activated lymphocyte subset that mounts antibody responses to T-cell-independent antigens through a Toll-like receptor (TLR)-amplified pathway involving transmembrane activator and CAML interactor (TACI). This receptor interacts with mTOR via the TLR adapter MyD88. The resulting mTOR activation instigates MZ B-cell proliferation, immunoglobulin G (IgG) class switching, and plasmablast differentiation through a rapamycin-sensitive pathway that integrates metabolic and antibody-inducing transcription programs, including NF-κB. Disruption of TACI-mTOR interaction by rapamycin, truncation of the MyD88-binding domain of TACI, or B-cell-conditional mTOR deficiency interrupts TACI signaling via NF-κB and cooperation with TLRs, thereby hampering IgG production to T-cell-independent antigens but not B-cell survival. Thus, mTOR drives innate-like antibody responses by linking proximal TACI signaling events with distal immunometabolic transcription programs." @default.
- W2767226775 created "2017-11-17" @default.
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- W2767226775 date "2017-11-13" @default.
- W2767226775 modified "2023-10-15" @default.
- W2767226775 title "mTOR intersects antibody-inducing signals from TACI in marginal zone B cells" @default.
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- W2767226775 doi "https://doi.org/10.1038/s41467-017-01602-4" @default.
- W2767226775 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5684130" @default.
- W2767226775 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29133782" @default.
- W2767226775 hasPublicationYear "2017" @default.