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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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Regulation of humoral and cellular gut immunity by lamina propria dendritic cells expressing Toll-like receptor 5

TL;DR: These findings demonstrate unique properties of LPDCs and the importance of TLR5 for adaptive immunity in the intestine and positively regulated the differentiation interleukin 17–producing T helper cells.
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Herpes simplex virus type 1 activates murine natural interferon-producing cells through toll-like receptor 9.

TL;DR: Though TLR9/MyD88-deficiency abrogates IPC responses to HSV-1 in vitro, mice lacking either MyD88 orTLR9 are capable of controlling HSV -1 replication in vivo after local infection, demonstrating that TLR 9- and MyD 88-independent pathways in cells other than IPCs can effectively compensate for defective IPC responders.
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Atg9a controls dsDNA-driven dynamic translocation of STING and the innate immune response

TL;DR: It is demonstrated that dynamic membrane traffic mediates the sequential translocation and assembly of STING, both of which are essential processes required for maximal activation of the innate immune response triggered by dsDNA.
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Involvement of Toll-like Receptor 3 in the Immune Response of Lung Epithelial Cells to Double-stranded RNA and Influenza A Virus *

TL;DR: It is demonstrated that TLR3 contributes directly to the immune response of respiratory epithelial cells to influenza A virus and dsRNA, and a molecular mechanism by which these stimuli induce epithelial cell activation is proposed.
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Microtubule-driven spatial arrangement of mitochondria promotes activation of the NLRP3 inflammasome

TL;DR: It is shown that microtubules mediated assembly of the NLRP3 inflammasome, and the creation of optimal sites for signal transduction by microtubule is required for activation of the entire NLRP2 inflammaome.