K
Kazumoto Murata
Researcher at Jichi Medical University
Publications - 150
Citations - 3595
Kazumoto Murata is an academic researcher from Jichi Medical University. The author has contributed to research in topics: Apoptosis & Interferon. The author has an hindex of 33, co-authored 135 publications receiving 3248 citations. Previous affiliations of Kazumoto Murata include International University of Health and Welfare & Mie University.
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Journal ArticleDOI
Hepatitis B virus-induced lipid alterations contribute to natural killer T cell-dependent protective immunity
Sebastian Zeissig,Kazumoto Murata,Lindsay Sweet,Jean Publicover,Zongyi Hu,Arthur Kaser,Arthur Kaser,Esther Bosse,Jahangir Iqbal,M. Mahmood Hussain,Katharina Balschun,Christoph Röcken,Alexander Arlt,Rainer Günther,Jochen Hampe,Stefan Schreiber,Jody L. Baron,D. Branch Moody,T. Jake Liang,Richard S. Blumberg +19 more
TL;DR: HBV-expressing hepatocytes produce endoplasmic reticulum (ER)-associated endogenous antigenic lipids including lysophospholipids that are generated by HBV-induced secretory phospholipases and that lead to activation of natural killer T (NKT) cells, which may contribute to control of HBV infection through sensing of HBv-induced modified self-lipids.
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Immunization with hepatitis C virus-like particles protects mice from recombinant hepatitis C virus-vaccinia infection
TL;DR: The results suggest that HCV-LPs can induce humoral and cellular immune responses that are protective in a surrogate HCV challenge model and that a strong cellular immunity provided by both CD4 and CD8 effector lymphocytes may be important for protection from HCV infection.
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Noninvasive estimation of liver fibrosis and response to interferon therapy by a serum fibrogenesis marker, YKL-40, in patients with HCV-associated liver disease.
Yukiko Saitou,Katsuya Shiraki,Yutaka Yamanaka,Yumi Yamaguchi,Tomoyuki Kawakita,Norihiko Yamamoto,Kazushi Sugimoto,Kazumoto Murata,Takeshi Nakano +8 more
TL;DR: YKL-40 may be a useful non-invasive serum marker to estimate the degree of liver fibrosis and to evaluate the efficacy of IFN therapies in patients with HCV-associated liver disease.
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Interleukin-1 and Tumor Necrosis Factor-α Trigger Restriction of Hepatitis B Virus Infection via a Cytidine Deaminase Activation-induced Cytidine Deaminase (AID)
Koichi Watashi,Guoxin Liang,Masashi Iwamoto,Hiroyuki Marusawa,Nanako Uchida,Takuji Daito,Kouichi Kitamura,Masamichi Muramatsu,Hirofumi Ohashi,Tomoko Kiyohara,Ryosuke Suzuki,Jisu Li,Shuping Tong,Yasuhito Tanaka,Kazumoto Murata,Hideki Aizaki,Takaji Wakita +16 more
TL;DR: It is found that pretreatment with IL-1β and TNFα remarkably reduced the host cell susceptibility to HBV infection, and this effect was mediated by activation of the NF-κB signaling pathway.
Journal ArticleDOI
Induction of IFN-λ3 as an additional effect of nucleotide, not nucleoside, analogues: a new potential target for HBV infection.
Kazumoto Murata,Mai Asano,Akihiro Matsumoto,Masaya Sugiyama,Nao Nishida,Eiji Tanaka,Taisuke Inoue,Minoru Sakamoto,Nobuyuki Enomoto,Takayoshi Shirasaki,Masao Honda,Shuichi Kaneko,Hiroyuki Gatanaga,Shinichi Oka,Yuki I. Kawamura,Taeko Dohi,Yasutaka Shuno,Hideaki Yano,Masashi Mizokami +18 more
TL;DR: It is discovered that the nucleotide analogues show an additional pharmacological effect by inducing IFN-λ3 production, which further induces ISGs and results in a reduction of HBsAg production.