S
Satoshi Kojo
Researcher at Hokkaido University
Publications - 39
Citations - 1514
Satoshi Kojo is an academic researcher from Hokkaido University. The author has contributed to research in topics: Natural killer T cell & T cell. The author has an hindex of 21, co-authored 39 publications receiving 1360 citations. Previous affiliations of Satoshi Kojo include University of Tsukuba & St. Marianna University School of Medicine.
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Journal ArticleDOI
Dysfunction of T cell receptor AV24AJ18+, BV11+ double-negative regulatory natural killer T cells in autoimmune diseases.
TL;DR: These findings strongly suggest that patients with autoimmune diseases can be divided into two groups (alpha-GalCer responders and nonresponders) and suggest that the reduced numbers of NKT cells in patients withimmune diseases may be due to an inadequate amount of alpha- GalCer-like natural ligands.
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IL-21-induced Bε cell apoptosis mediated by natural killer T cells suppresses IgE responses
Michishige Harada,Kumiko Magara-Koyanagi,Hiroshi Watarai,Yuko Nagata,Yasuyuki Ishii,Satoshi Kojo,Shigetoshi Horiguchi,Yoshitaka Okamoto,Toshinori Nakayama,Nobutaka Suzuki,Wen Chen Yeh,Shizuo Akira,Hiroshi Kitamura,Osamu Ohara,Ken-ichiro Seino,Masaru Taniguchi +15 more
TL;DR: It is demonstrated that natural killer T (NKT) cells in mice and humans play a crucial role in the BCG-induced suppression of IgE responses, providing new insight into the therapeutic effect of BCG in allergic diseases.
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Vα14 NK T cell–triggered IFN-γ production by Gr-1+CD11b+ cells mediates early graft loss of syngeneic transplanted islets
Yohichi Yasunami,Satoshi Kojo,Hiroshi Kitamura,Atsushi Toyofuku,Atsushi Toyofuku,Masayuki Satoh,Masahiko Nakano,Kentaroh Nabeyama,Yoshiichiroh Nakamura,Nobuhide Matsuoka,Seiyo Ikeda,Masao Tanaka,Junko Ono,Naoki Nagata,Osamu Ohara,Masaru Taniguchi +15 more
TL;DR: This study elucidates, for the first time, the crucial role of Gr-1+CD11b+ cells and the IFN-γ they produce in islet graft rejection and suggests a novel approach to improving transplantation efficiency through the modulation of Vα14 NKT cell function.
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Cutting edge: critical role of CXCL16/CXCR6 in NKT cell trafficking in allograft tolerance.
Xiaofeng Jiang,Takeshi Shimaoka,Satoshi Kojo,Michishige Harada,Hiroshi Watarai,Hiroshi Wakao,Nobuhiro Ohkohchi,Shin Yonehara,Masaru Taniguchi,Ken-ichiro Seino +9 more
TL;DR: Blocking of the interaction between the chemokine receptor, CXCR6, and CXCL16, resulted in the failure to maintain graft tolerance and thus in the induction of acceleration of graft rejection, demonstrating the unique role of CxCL16 and CxCR6 molecules in the maintenance of cardiac allograft tolerance mediated by NKT cells.
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Induction of Regulatory Properties in Dendritic Cells by Vα14 NKT Cells
Satoshi Kojo,Ken-ichiro Seino,Michishige Harada,Hiroshi Watarai,Hiroshi Wakao,Tetsuro Uchida,Toshinori Nakayama,Masaru Taniguchi +7 more
TL;DR: These DCs showed an ability to suppress the development of experimental allergic encephalomyelitis by generating IL-10-producing regulatory CD4 T cells in vivo and contribute to explaining how Vα14 NKT cells regulate the immune responses in vivo.