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Shizuo Akira

Researcher at Osaka University

Publications -  1330
Citations -  344469

Shizuo Akira is an academic researcher from Osaka University. The author has contributed to research in topics: Innate immune system & Immune system. The author has an hindex of 261, co-authored 1308 publications receiving 320561 citations. Previous affiliations of Shizuo Akira include University of California, Berkeley & Wakayama Medical University.

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Inhibition of RIG-I-Dependent Signaling to the Interferon Pathway during Hepatitis C Virus Expression and Restoration of Signaling by IKKε

TL;DR: The partial restoration of the capacity of the host cell to transcribe IFN-β indicates that IKKε expression is able to bypass the HCV-mediated inhibition and restore the innate antiviral response.
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Toll-like receptor ligands synergize through distinct dendritic cell pathways to induce T cell responses: Implications for vaccines

TL;DR: An underlying TLR mechanism governing the functional, nonrandom interplay among TLRs for recognition of combinatorial ligands that may be dangerous to the host is revealed, providing important guidance for design of novel synergistic molecular vaccine adjuvants.
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Activation of TBK1 and IKKε Kinases by Vesicular Stomatitis Virus Infection and the Role of Viral Ribonucleoprotein in the Development of Interferon Antiviral Immunity

TL;DR: Examination of the activation of TBK1 and IKKε kinases by vesicular stomatitis virus (VSV) infection in human lung epithelial A549 cells suggests that intracellular RNP formation contributes to the early recognition of VSV infection, activates the catalytic activity ofTBK1, and induces transcriptional upregulation of IKKα in epithelial cells.
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Murine dendritic cell type I IFN production induced by human IgG-RNA immune complexes is IFN regulatory factor (IRF)5 and IRF7 dependent and is required for IL-6 production.

TL;DR: It is shown that sera and purified IgG from lupus patients activate mouse DCs to produceIFN-α, IFN-β, and IL-6 and up-regulate costimulatory molecules in a FcγR-dependent manner, indicating the need for a type I IFn-dependent feedback loop in the production of inflammatory cytokines.