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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

The Malarial Metabolite Hemozoin and Its Potential Use as a Vaccine Adjuvant

TL;DR: The potential application of hemozoin crystals as an adjuvant may provide insights into the molecular mechanisms involved in immune responses to malarial infection and provide a rationale for the design of vaccines against malaria as well as other immunological disorders such as allergies.
Journal ArticleDOI

TAK1 modulates satellite stem cell homeostasis and skeletal muscle repair.

TL;DR: It is demonstrated that transforming growth factor-β-activated kinase 1 (TAK1) is important in satellite stem cell homeostasis and function and suggested that TAK1 is required for maintaining the pool of satellite stem cells and for regenerative myogenesis.
Book ChapterDOI

Regulation of expression of the interleukin 6 gene: structure and function of the transcription factor NF-IL6.

TL;DR: Findings indicate that NF-IL6 may be an important transcription factor on the signal transduction pathways of IL-1 and IL-6.
Journal ArticleDOI

Muramyl Dipeptide Induces NOD2-Dependent Ly6Chigh Monocyte Recruitment to the Lungs and Protects Against Influenza Virus Infection

TL;DR: It is shown that MDP treatment of mice infected with Influenza A virus significantly reduces mortality, viral load and pulmonary inflammation in a NOD2-dependent manner and identifies the Nod2 pathway as a potential therapeutic target against IAV.
Journal ArticleDOI

Toxoplasma gondii–derived heat shock protein HSP70 functions as a B cell mitogen

TL;DR: The involvement of TLR4 in the TgHSP70-induced proliferative responses of spleen cells was observed in MyD88−/− mice, indicating that the MyD 88 molecule was involved in LPS-induced proliferation but not in T gondii–infected mice, and induced the proliferation of B cells but not T cells.