S
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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Microsomal prostaglandin E synthase-1 is a critical factor of stroke-reperfusion injury
TL;DR: The induction of microsomal PGE synthase 1 (mPGES-1) is demonstrated, an inducible terminal enzyme for PGE(2) synthesis, in neurons, microglia, and endothelial cells in the cerebral cortex after transient focal ischemia in mice, suggesting that mPGes-1 may be a critical determinant of postischemic neurological dysfunctions and a valuable therapeutic target for treatment of human stroke.
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Cancer therapies activate RIG-I-like receptor pathway through endogenous non-coding RNAs.
Diana Rose E. Ranoa,A. Parekh,Sean P. Pitroda,Xiaona Huang,Thomas E. Darga,Anthony C. Wong,Lei Huang,Jorge Andrade,Jonathan P. Staley,Takashi Satoh,Shizuo Akira,Ralph R. Weichselbaum,Nikolai N. Khodarev +12 more
TL;DR: These findings suggest that the physiologic responses to radio-/chemo-therapy converge on an antiviral program in recruitment of the RLR pathway by a sncRNA-dependent activation of RIG-I which commences cytotoxic IFN signaling.
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IL-6 and IL-10 induction from dendritic cells in response to Mycobacterium tuberculosis is predominantly dependent on TLR2-mediated recognition.
TL;DR: The data presented here provide a mechanistic insight for the contribution of TLR2 and TLR4 to tuberculosis disease progression and offer strategies for regulating IL-6 and IL-10 production in dendritic cell-based vaccine strategies.
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Pleiotropic function of Toll-like receptors.
Tsuneyasu Kaisho,Shizuo Akira +1 more
TL;DR: A group of type I transmembrane proteins, Toll-like receptors (TLRs) discriminate various microorganism-associated molecular structures that can function as immune adjuvants and provide critical information for manipulating the host defense mechanism.
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Enterocyte-Derived TAK1 Signaling Prevents Epithelium Apoptosis and the Development of Ileitis and Colitis
Rie Kajino-Sakamoto,Maiko Inagaki,Elisabeth Lippert,Shizuo Akira,Sylvie Robine,Kunihiro Matsumoto,Christian Jobin,Jun Ninomiya-Tsuji +7 more
TL;DR: Enterocyte apoptosis and intestinal inflammation were strongly attenuated when enterocyte-specific constitutive TAK1-deleted mice were crossed to TNF receptor 1−/− mice, and it is proposed that aberration in Tak1 signaling might disrupt intestinal homeostasis and favor the development of inflammatory disease.