K
Katsuaki Hoshino
Researcher at Kagawa University
Publications - 84
Citations - 33652
Katsuaki Hoshino is an academic researcher from Kagawa University. The author has contributed to research in topics: Toll-like receptor & TLR4. The author has an hindex of 47, co-authored 80 publications receiving 32261 citations. Previous affiliations of Katsuaki Hoshino include Hokkaido University & Wakayama Medical University.
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Journal ArticleDOI
A Toll-like receptor recognizes bacterial DNA.
Hiroaki Hemmi,Osamu Takeuchi,Taro Kawai,Tsuneyasu Kaisho,Shintaro Sato,Hideki Sanjo,Makoto Matsumoto,Katsuaki Hoshino,Hermann Wagner,Kiyoshi Takeda,Shizuo Akira +10 more
TL;DR: It is shown that cellular response to CpG DNA is mediated by a Toll-like receptor, TLR9, and vertebrate immune systems appear to have evolved a specific Toll- like receptor that distinguishes bacterial DNA from self-DNA.
Journal Article
Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product.
Katsuaki Hoshino,Osamu Takeuchi,Taro Kawai,Hideki Sanjo,Tomohiko Ogawa,Yoshifumi Takeda,Kiyoshi Takeda,Shizuo Akira +7 more
TL;DR: It is demonstrated that TLR4 is the gene product that regulates LPS response, and a single point mutation of the amino acid that is highly conserved among the IL-1/Toll receptor family is found.
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Differential roles of TLR2 and TLR4 in recognition of gram-negative and gram-positive bacterial cell wall components.
Osamu Takeuchi,Katsuaki Hoshino,Taro Kawai,Hideki Sanjo,Haruhiko Takada,Tomohiko Ogawa,Kiyoshi Takeda,Shizuo Akira +7 more
TL;DR: It is demonstrated that TLR2 and TLR4 recognize different bacterial cell wall components in vivo andTLR2 plays a major role in Gram-positive bacterial recognition.
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Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway.
Masahiro Yamamoto,Shintaro Sato,Hiroaki Hemmi,Katsuaki Hoshino,Tsuneyasu Kaisho,Hideki Sanjo,Osamu Takeuchi,Masanaka Sugiyama,Masaru Okabe,Kiyoshi Takeda,Shizuo Akira +10 more
TL;DR: It is shown that TRIF is essential for TLR3- and TLR4-mediated signaling pathways facilitating mammalian antiviral host defense and complete loss of nuclear factor kappa B activation in response toTLR4 stimulation is demonstrated.
Journal ArticleDOI
Small anti-viral compounds activate immune cells via the TLR7 MyD88-dependent signaling pathway.
Hiroaki Hemmi,Tsuneyasu Kaisho,Osamu Takeuchi,Shintaro Sato,Hideki Sanjo,Katsuaki Hoshino,Takao Horiuchi,Hideyuki Tomizawa,Kiyoshi Takeda,Shizuo Akira +9 more
TL;DR: It is shown that the imidazoquinolines activate immune cells via the Toll-like receptor 7 (TLR7)-MyD88–dependent signaling pathway, and that neither MyD88- nor TLR7-deficient mice showed any inflammatory cytokine production by macrophages, proliferation of splenocytes or maturation of dendritic cells.