M
Misako Matsumoto
Researcher at Hokkaido University
Publications - 294
Citations - 19179
Misako Matsumoto is an academic researcher from Hokkaido University. The author has contributed to research in topics: Toll-like receptor & Innate immune system. The author has an hindex of 69, co-authored 290 publications receiving 17460 citations. Previous affiliations of Misako Matsumoto include Nara Institute of Science and Technology & Aomori University.
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Journal ArticleDOI
TICAM-1, an adaptor molecule that participates in Toll-like receptor 3-mediated interferon-beta induction.
TL;DR: This work has identified an alternative adaptor, designated Toll-interleukin 1 receptor domain (TIR)-containing adaptor molecule (TICAM)-1, that can physically bind the TIR domain of TLR3 and activate the IFN-β promoter in response to poly(I):poly(C).
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Subcellular Localization of Toll-Like Receptor 3 in Human Dendritic Cells
Misako Matsumoto,Kenji Funami,Masako Tanabe,Hiroyuki Oshiumi,Masashi Shingai,Yoshiyuki Seto,Akitsugu Yamamoto,Tsukasa Seya +7 more
TL;DR: Immunoelectron microscopic analysis revealed that TLR3, when stably expressed in the murine B cell line Ba/F3, was specifically accumulated in multivesicular bodies, a subcellular compartment situated in endocytic trafficking pathways, which may reflect participation of cell type-specific multiple pathways in antiviral IFN induction viaTLR3.
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TLR3: interferon induction by double-stranded RNA including poly(I:C).
Misako Matsumoto,Tsukasa Seya +1 more
TL;DR: Current knowledge on TLR3 is summarized and its possible role in innate and adaptive immunity is discussed and involved in activation of NK cells and CTLs by myeloid DCs suggests thatTLR3 serves as an inducer of cellular immunity sensing viral infection rather than a simple IFN inducer.
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Aberrant PD-L1 expression through 3′-UTR disruption in multiple cancers
Keisuke Kataoka,Yuichi Shiraishi,Yohei Takeda,Seiji Sakata,Misako Matsumoto,Seiji Nagano,Takuya Maeda,Yasunobu Nagata,Akira Kitanaka,Seiya Mizuno,Hiroko Tanaka,Kenichi Chiba,Satoshi Ito,Yosaku Watatani,Nobuyuki Kakiuchi,Hiromichi Suzuki,Tetsuichi Yoshizato,Kenichi Yoshida,Masashi Sanada,Hidehiro Itonaga,Yoshitaka Imaizumi,Yasushi Totoki,Wataru Munakata,Hiromi Nakamura,Natsuko Hama,Kotaro Shide,Yoko Kubuki,Tomonori Hidaka,Takuro Kameda,Kyoko Masuda,Nagahiro Minato,Koichi Kashiwase,Koji Izutsu,Akifumi Takaori-Kondo,Yasushi Miyazaki,Satoru Takahashi,Tatsuhiro Shibata,Hiroshi Kawamoto,Yoshiki Akatsuka,Kazuya Shimoda,Kengo Takeuchi,Tsukasa Seya,Satoru Miyano,Seishi Ogawa +43 more
TL;DR: A unique genetic mechanism of immune escape caused by structural variations (SVs) commonly disrupting the 3' region of the PD-L1 gene is shown, supporting the role of relevant SVs in clonal selection through immune evasion and suggesting that PD-l1 3'-UTR disruption could serve as a genetic marker to identify cancers that actively evade anti-tumour immunity through PD- L1 overexpression.
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Establishment of a monoclonal antibody against human Toll-like receptor 3 that blocks double-stranded RNA-mediated signaling.
TL;DR: The mAb against TLR3 reported herein may serve as a regulator for virus-mediated immune response via an alternative pathway involving the dsRNA-TLR3 recognition which might occur on host cells.