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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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Journal ArticleDOI
Viral Infection Augments Nod1/2 Signaling to Potentiate Lethality Associated with Secondary Bacterial Infections
Yun Gi Kim,Jong Hwan Park,Thornik Reimer,Darren P. Baker,Taro Kawai,Himanshu Kumar,Himanshu Kumar,Shizuo Akira,Christiane E. Wobus,Gabriel Núñez +9 more
TL;DR: It is shown that crosstalk between type I IFNs and Nod1/Nod2 signaling promotes bacterial recognition, but induces harmful effects in the virally infected host.
Journal ArticleDOI
The role of Toll-like receptors and MyD88 in innate immune responses.
TL;DR: Activation of NF-κB and MAP kinases was induced in response to LPS even in the absence of MyD88, which indicates the existence of a MyD 88-independent pathway and is involved in LPS-induced maturation of dendritic cells (DCs).
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Soluble CD14 enriched in colostrum and milk induces B cell growth and differentiation
Dominik Filipp,Kamel Alizadeh-Khiavi,Christopher D. Richardson,Anthony Palma,Nethnapha Paredes,Osamu Takeuchi,Shizuo Akira,Michael Julius +7 more
TL;DR: The results presented establish sCD14 as a naturally occurring soluble B cell mitogen of mammalian origin and its administration to neonatal mice enhances Ig secretion.
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Toll-Like Receptor 9-Dependent Activation of Myeloid Dendritic Cells by Deoxynucleic Acids from Candida albicans
Akiko Miyazato,Akiko Miyazato,Kiwamu Nakamura,Natsuo Yamamoto,Héctor M. Mora-Montes,Misuzu Tanaka,Yuzuru Abe,Daiki Tanno,Ken Inden,Xiao Gang,Keiko Ishii,Kiyoshi Takeda,Shizuo Akira,Shinobu Saijo,Yoichiro Iwakura,Yoshiyuki Adachi,Naohito Ohno,Kotaro Mitsutake,Neil A. R. Gow,Mitsuo Kaku,Kazuyoshi Kawakami +20 more
TL;DR: Results suggested that C. albicans DNA activated BM-DCs through a TLR9-mediated signaling pathway using a mechanism independent of the unmethylated CpG motif, which suggested that the innate immune system of humans recognizes the human pathogenic fungus CandidaAlbicans via sugar polymers present in the cell wall.
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Myeloid Differentiation Factor 88 (MyD88)-Deficiency Increases Risk of Diabetes in Mice
TL;DR: The present finding of an unexpected role for MyD88 in preventing diabetes may provide a potential novel target/strategy for treating metabolic syndrome.