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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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The roles of Toll-like receptor 9, MyD88, and DNA-dependent protein kinase catalytic subunit in the effects of two distinct CpG DNAs on dendritic cell subsets.

TL;DR: It is demonstrated that the TLR9-MyD88 signaling pathway is essential for all DC responses to both types of CpG DNAs, including splenic and in vitro bone marrow-derived DCs.
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Viral infections activate types I and III interferon genes through a common mechanism.

TL;DR: Results strongly suggest that types I and III IFN genes are regulated by a common mechanism, including a cluster of interferon regulatory factor-binding sites and a NF-κB-binding site essential for gene activation by the virus.
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Reduced atherosclerosis in interleukin-18 deficient apolipoprotein E-knockout mice

TL;DR: These data show reduced atherosclerosis and Th1 activity in spite of increased serum cholesterol in IL-18 deficient apoE(-/-) mice, which support a proatherogenic role for IL- 18.
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The Salmonella Pathogenicity Island (SPI)-2 and SPI-1 Type III Secretion Systems Allow Salmonella Serovar typhimurium to Trigger Colitis via MyD88-Dependent and MyD88-Independent Mechanisms

TL;DR: S. typhimurium can use two independent mechanisms to elicit colitis in vivo: SPI-1-dependent and MyD 88-independent signaling to epithelial cells and SPI-2-dependent intracellular proliferation in the lamina propria triggering MyD88-dependent innate immune responses.
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Selective contribution of IFN-α/β signaling to the maturation of dendritic cells induced by double-stranded RNA or viral infection

TL;DR: It is shown that IFN-α/β signaling is selectively required for the maturation of DCs induced by double-stranded RNA or viral infection in vitro, and that the DCs stimulated in vivo by these agents can migrate into the T cell zone of the spleen but fail to mature without the IFN signal.