T
Tasuku Honjo
Researcher at Kyoto University
Publications - 727
Citations - 94745
Tasuku Honjo is an academic researcher from Kyoto University. The author has contributed to research in topics: Gene & Cytidine deaminase. The author has an hindex of 141, co-authored 712 publications receiving 88428 citations. Previous affiliations of Tasuku Honjo include Kumamoto University & University of Medicine and Dentistry of New Jersey.
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Journal ArticleDOI
Engagement of the PD-1 immunoinhibitory receptor by a novel B7 family member leads to negative regulation of lymphocyte activation.
Gordon J. Freeman,Andrew J. Long,Yoshiko Iwai,Karen Bourque,Tatyana Chernova,Hiroyuki Nishimura,Lori Fitz,Nelly Malenkovich,Taku Okazaki,Michael C. Byrne,Heidi F. Horton,Lynette A. Fouser,Laura L. Carter,Vincent Ling,Michael R Bowman,Beatriz M. Carreno,Mary Collins,Clive Wood,Tasuku Honjo +18 more
TL;DR: It is reported here that the ligand of PD-1 (PD-L1), an immunoinhibitory receptor expressed by activated T cells, B cells, and myeloid cells, is a member of the B7 gene family.
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Class Switch Recombination and Hypermutation Require Activation-Induced Cytidine Deaminase (AID), a Potential RNA Editing Enzyme
Masamichi Muramatsu,Kazuo Kinoshita,Sidonia Fagarasan,Shuichi Yamada,Yoichi Shinkai,Tasuku Honjo +5 more
TL;DR: Results suggest that AID may be involved in regulation or catalysis of the DNA modification step of both class switching and somatic hypermutation in CH12F3-2 B lymphoma.
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PD-L2 is a second ligand for PD-1 and inhibits T cell activation
Yvette Latchman,Clive Wood,Tatyana Chernova,Divya Chaudhary,Madhuri Borde,Irene Chernova,Yoshiko Iwai,Andrew J. Long,Julia A. Brown,Raquel A. Nunes,Edward A. Greenfield,Karen Bourque,Vassiliki A. Boussiotis,Laura L. Carter,Beatriz M. Carreno,Nelly Malenkovich,Hiroyuki Nishimura,Taku Okazaki,Tasuku Honjo,Arlene H. Sharpe,Gordon J. Freeman +20 more
TL;DR: These studies show overlapping functions of PD-L1 andPD-L2 and indicate a key role for the PD- L–PD-1 pathway in regulating T cell responses.
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Involvement of PD-L1 on tumor cells in the escape from host immune system and tumor immunotherapy by PD-L1 blockade
TL;DR: The results suggest that the expression of PD-L1 can serve as a potent mechanism for potentially immunogenic tumors to escape from host immune responses and that blockade of interaction between PD-1 andPD-L may provide a promising strategy for specific tumor immunotherapy.
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Induced expression of PD-1, a novel member of the immunoglobulin gene superfamily, upon programmed cell death.
TL;DR: The results suggest that activation of the PD‐1 gene may be involved in the classical type of programmed cell death.