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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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Ubc13 maintains the suppressive function of regulatory T cells and prevents their conversion into effector-like T cells

TL;DR: It is found that Treg cell–specific ablation of Ubc13, a Lys63 (K63)-specific ubiquitin-conjugating enzyme, caused aberrant T cell activation and autoimmunity, and suggests that the Ubc 13-IKK signaling axis regulates the molecular program that maintains TReg cell function and prevents Treg cells from acquiring inflammatory phenotypes.
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Requirement for TLR9 in the Immunomodulatory Activity of Propionibacterium acnes

TL;DR: It is shown in this study that TLR9 is crucial in generating the characteristic effects of killed P. acnes priming in the spleen, such as extramedullary hemopoiesis and organ enlargement, and granuloma formation in the liver.
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Cutting edge: bacterial infection induces hematopoietic stem and progenitor cell expansion in the absence of TLR signaling.

TL;DR: In vivo in vivo HSPC responses to bacterial infection are complex and not absolutely dependent upon key inflammatory signaling pathways, as shown in this study.
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A selective contribution of the RIG-I-like receptor pathway to type I interferon responses activated by cytosolic DNA

TL;DR: It is demonstrated that overexpression of otherwise IFN-inducible RIG-I or MDA5 in IFN signal-deficient cells results in a marked enhancement of type I IFN gene induction upon cytosolic DNA stimulation, while in their absence the induction is impaired.
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Inhibitory effect of Toll-like receptor 4 on fusion between phagosomes and endosomes/lysosomes in macrophages.

TL;DR: Results collectively indicate that TLR4 negatively regulates the degradation of engulfed cells in macrophages via a pathway independent of NF-κB.