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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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Interleukin-6 and its receptor: a paradigm for cytokines
TL;DR: Many cytokines and cytokine receptors involved in the regulation of hematopoiesis, immune responses, and inflammation have been identified and characterized at the molecular level and are now more clearly understood on the basis of their molecular structures.
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Toll-like receptor function and signaling.
Tsuneyasu Kaisho,Shizuo Akira +1 more
TL;DR: Understanding molecular mechanisms on Toll-like receptors should be quite useful in the development of therapeutic maneuvers against allergy and autoimmune diseases.
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Identification of a key pathway required for the sterile inflammatory response triggered by dying cells
TL;DR: It is suggested that inhibiting the IL-1R–Myd88 pathway in vivo could block the damage from acute inflammation that occurs in response to sterile cell death, and do so in a way that might not compromise tissue repair or host defense against pathogens.
Journal Article
IL-12 up-regulates IL-18 receptor expression on T cells, Th1 cells, and B cells: synergism with IL-18 for IFN-gamma production.
Tomohiro Yoshimoto,Kiyoshi Takeda,Takashi Tanaka,Kazunobu Ohkusu,Shin-ichiro Kashiwamura,Haruki Okamura,Shizuo Akira,Kenji Nakanishi +7 more
TL;DR: It is shown that IL-12 and IL-18 promptly and synergistically induce T and B cells to develop into IFN-gamma-producing cells without engaging their Ag receptors and the mechanism underlying differences inIL-18 responsiveness between Th1 and Th2 cells is studied.
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Toll-Like Receptors on Hematopoietic Progenitor Cells Stimulate Innate Immune System Replenishment
Yoshinori Nagai,Karla P. Garrett,Shoichiro Ohta,Uleng Bahrun,Taku Kouro,Shizuo Akira,Kiyoshi Takatsu,Paul W. Kincade +7 more
TL;DR: It is shown that TLRs and their coreceptors were expressed by multipotential hematopoietic stem cells, whose cell cycle entry was triggered by TLR ligation, and the preferential pathogen-mediated stimulation of myeloid differentiation pathways may provide a means for rapid replenishment of the innate immune system during infection.