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38 results on '"Koyama-Nasu, Ryo"'

1. The pathogenetic significance of exhausted T cells in a mouse model of mature B cell neoplasms

Author

Shibamiya, Asuka, Miyamoto-Nagai, Yurie, Koide, Shuhei, Oshima, Motohiko, Rizq, Ola, Aoyama, Kazumasa, Nakajima-Takagi, Yaeko, Kato, Rei, Kayamori, Kensuke, Isshiki, Yusuke, Oshima-Hasegawa, Nagisa, Muto, Tomoya, Tsukamoto, Shokichi, Takeda, Yusuke, Koyama-Nasu, Ryo, Chiba, Tetsuhiro, Honda, Hiroaki, Yokote, Koutaro, Iwama, Atsushi, Sakaida, Emiko, and Mimura, Naoya

Published
2023
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7. Figure S1, S2, S3, S4, S5, S6, S7, S8, S9, S10, S11 from CD69 Imposes Tumor-Specific CD8+ T-cell Fate in Tumor-Draining Lymph Nodes

Author

Koyama-Nasu, Ryo, primary, Kimura, Motoko Y., primary, Kiuchi, Masahiro, primary, Aoki, Ami, primary, Wang, Yangsong, primary, Mita, Yukiyoshi, primary, Hasegawa, Ichita, primary, Endo, Yukihiro, primary, Onodera, Atsushi, primary, Hirahara, Kiyoshi, primary, Motohashi, Shinichiro, primary, and Nakayama, Toshinori, primary

Published
2023
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9. CD69 imposes tumor-specific CD8+ T-cell fate in tumor-draining lymph nodes

Author

Koyama-Nasu, Ryo, primary, Kimura, Motoko Y., additional, Kiuchi, Masahiro, additional, Aoki, Ami, additional, Wang, Yangsong, additional, Mita, Yukiyoshi, additional, Hasegawa, Ichita, additional, Endo, Yukihiro, additional, Onodera, Atsushi, additional, Hirahara, Kiyoshi, additional, Motohashi, Shinichiro, additional, and Nakayama, Toshinori, additional

Published
2023
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12. Exhausted T Cells Characterized By Upregulation of Specific Transcription Factors Are Increased in a Mouse Model of De Novo Mature B Cell Neoplasms

Author

Shibamiya, Asuka, primary, Mimura, Naoya, additional, Miyamoto-Nagai, Yurie, additional, Koide, Shuhei, additional, Oshima, Motohiko, additional, Rizq, Ola, additional, Aoyama, Kazumasa, additional, Nakajima-Takagi, Yaeko, additional, Kayamori, Kensuke, additional, Isshiki, Yusuke, additional, Oshima-Hasegawa, Nagisa, additional, Muto, Tomoya, additional, Tsukamoto, Shokichi, additional, Takeda, Yusuke, additional, Koyama-Nasu, Ryo, additional, Chiba, Tetsuhiro, additional, Honda, Hiroaki, additional, Yokote, Koutaro, additional, Iwama, Atsushi, additional, and Sakaida, Emiko, additional

Published
2022
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13. 5-Hydroxymethylcytosine Plays a Critical Role in Glioblastomagenesis by Recruiting the CHTOP-Methylosome Complex

Author

Takai, Hiroki, Masuda, Koji, Sato, Tomohiro, Sakaguchi, Yuriko, Suzuki, Takeo, Suzuki, Tsutomu, Koyama-Nasu, Ryo, Nasu-Nishimura, Yukiko, Katou, Yuki, Ogawa, Haruo, Morishita, Yasuyuki, Kozuka-Hata, Hiroko, Oyama, Masaaki, Todo, Tomoki, Ino, Yasushi, Mukasa, Akitake, Saito, Nobuhito, Toyoshima, Chikashi, Shirahige, Katsuhiko, and Akiyama, Tetsu

Published
2014
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18. cellular and molecular basis of CD69 function in anti-tumor immunity.

Author

Koyama-Nasu, Ryo, Wang, Yangsong, Hasegawa, Ichita, Endo, Yukihiro, Nakayama, Toshinori, and Kimura, Motoko Y

Subjects
*IMMUNE response, *IMMUNITY, *APOPTOSIS, *LYMPHOID tissue, *T cells
Abstract

Cancer immunotherapy utilizes our immune system to attack cancer cells and is an extremely promising strategy for cancer treatment. Although immune-checkpoint blockade, such as anti-PD-1 (programmed cell death 1) antibody, has demonstrated significant enhancement of anti-tumor immunity and has induced notable clinical outcomes, its response rates remain low, and adverse effects are always a matter of concern; therefore, new targets for cancer immunotherapy are always desired. In this situation, new concepts are needed to fuel the investigation of new target molecules for cancer immunotherapy. We propose that CD69 is one such target molecule. CD69 is known to be an activation marker of leukocytes and is also considered a crucial regulator of various immune responses through its interacting proteins. CD69 promotes T-cell retention in lymphoid tissues via sphingosine-1-phosphate receptor 1 (S1P1) internalization and also plays roles in the pathogenesis of inflammatory disorders through interacting with its functional ligands Myl9/12 (myosin light chains 9, 12a and 12b). In anti-tumor immunity, CD69 is known to be expressed on T cells in the tumor microenvironment (TME) and tumor-draining lymph nodes (TDLNs). We revealed that CD69 negatively regulates the effector function of intratumoral T cells and importantly controls the 'exhaustion' of CD8 T cells. In addition, we and others showed that either CD69 deficiency or the administration of anti-CD69 monoclonal antibody enhances anti-tumor immunity. Thus, CD69 is an attractive target for cancer immunotherapy. [ABSTRACT FROM AUTHOR]

Published
2022
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19. JHDM1B/FBXL10 is a nucleolar protein that represses transcription of ribosomal RNA genes

Author

Frescas, David, Guardavaccaro, Daniele, Bassermann, Florian, Koyama-Nasu, Ryo, and Pagano, Michele

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): David Frescas [1]; Daniele Guardavaccaro [1]; Florian Bassermann [1]; Ryo Koyama-Nasu [1]; Michele Pagano (corresponding author) [1] JHDM1B is an evolutionarily conserved and ubiquitously expressed member of the JHDM [...]

Published
2007
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20. CD1d expression in glioblastoma is a promising target for NKT cell-based cancer immunotherapy

Author

Hara, Ayaka, primary, Koyama-Nasu, Ryo, additional, Takami, Mariko, additional, Toyoda, Takahide, additional, Aoki, Takahiro, additional, Ihara, Fumie, additional, Kobayashi, Masayoshi, additional, Hirono, Seiichiro, additional, Matsutani, Tomoo, additional, Nakayama, Toshinori, additional, Iwadate, Yasuo, additional, and Motohashi, Shinichiro, additional

Published
2020
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21. Essential Role for CD30-Transglutaminase 2 Axis in Memory Th1 and Th17 Cell Generation

Author

Suzuki, Akane S., primary, Yagi, Ryoji, additional, Kimura, Motoko Y., additional, Iwamura, Chiaki, additional, Shinoda, Kenta, additional, Onodera, Atsushi, additional, Hirahara, Kiyoshi, additional, Tumes, Damon J., additional, Koyama-Nasu, Ryo, additional, Iismaa, Siiri E., additional, Graham, Robert M., additional, Motohashi, Shinichiro, additional, and Nakayama, Toshinori, additional

Published
2020
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22. Activated invariant natural killer T cells directly recognize leukemia cells in a CD1d‐independent manner

Author

Aoki, Takahiro, primary, Takami, Mariko, additional, Takatani, Tomozumi, additional, Motoyoshi, Kiwamu, additional, Ishii, Ayana, additional, Hara, Ayaka, additional, Toyoda, Takahide, additional, Okada, Reona, additional, Hino, Moeko, additional, Koyama‐Nasu, Ryo, additional, Kiuchi, Masahiro, additional, Hirahara, Kiyoshi, additional, Kimura, Motoko Y., additional, Nakayama, Toshinori, additional, Shimojo, Naoki, additional, and Motohashi, Shinichiro, additional

Published
2020
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23. Invariant NKT Cells Recognize Leukemia Cells with T-Cell and NK Receptors in a CD1d-Independent Manner

Author

Aoki, Takahiro, primary, Takami, Mariko, additional, Takatani, Tomozumi, additional, Motoyoshi, Kiwamu, additional, Ishii, Ayana, additional, Hara, Ayaka, additional, Toyoda, Takahide, additional, Okada, Reona, additional, Hino, Moeko, additional, Koyama-Nasu, Ryo, additional, Kiuchi, Masahiro, additional, Hirahara, Kiyoshi, additional, Nakayama, Toshinori, additional, Shimojo, Naoki, additional, and Motohashi, Shinichiro, additional

Published
2019
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24. SIRT 2‐mediated inactivation of p73 is required for glioblastoma tumorigenicity

Author

Funato, Kosuke, primary, Hayashi, Tomoatsu, additional, Echizen, Kanae, additional, Negishi, Lumi, additional, Shimizu, Naomi, additional, Koyama‐Nasu, Ryo, additional, Nasu‐Nishimura, Yukiko, additional, Morishita, Yasuyuki, additional, Tabar, Viviane, additional, Todo, Tomoki, additional, Ino, Yasushi, additional, Mukasa, Akitake, additional, Saito, Nobuhito, additional, and Akiyama, Tetsu, additional

Published
2018
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29. PCDH10 is required for the tumorigenicity of glioblastoma cells

Author

Echizen, Kanae, Nakada, Mitsutoshi, Hayashi, Tomoatsu, Sabit, Hemragul, Furuta, Takuya, Nakai, Miyuki, Koyama-Nasu, Ryo, Nishimura, Yukiko, Taniue, Kenzui, Morishita, Yasuyuki, Hirano, Shinji, Terai, Kenta, Todo, Tomoki, Ino, Yasushi, Mukasa, Akitake, Takayanagi, Shunsaku, Ohtani, Ryohei, Saito, Nobuhito, and Akiyama, Tetsu

Published
2014
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30. Exhausted T Cells Characterized By Upregulation of Specific Transcription Factors Are Increased in a Mouse Model of De NovoMature B Cell Neoplasms

Author

Shibamiya, Asuka, Mimura, Naoya, Miyamoto-Nagai, Yurie, Koide, Shuhei, Oshima, Motohiko, Rizq, Ola, Aoyama, Kazumasa, Nakajima-Takagi, Yaeko, Kayamori, Kensuke, Isshiki, Yusuke, Oshima-Hasegawa, Nagisa, Muto, Tomoya, Tsukamoto, Shokichi, Takeda, Yusuke, Koyama-Nasu, Ryo, Chiba, Tetsuhiro, Honda, Hiroaki, Yokote, Koutaro, Iwama, Atsushi, and Sakaida, Emiko

Published
2022
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31. The Cancer Stem Cell Marker CD133 Interacts with Plakoglobin and Controls Desmoglein-2 Protein Levels

Author

Koyama-Nasu, Ryo, primary, Takahashi, Rina, additional, Yanagida, Satoshi, additional, Nasu-Nishimura, Yukiko, additional, Oyama, Masaaki, additional, Kozuka-Hata, Hiroko, additional, Haruta, Ryo, additional, Manabe, Emi, additional, Hoshino-Okubo, Akemi, additional, Omi, Hiroko, additional, Yanaihara, Nozomu, additional, Okamoto, Aikou, additional, Tanaka, Tadao, additional, and Akiyama, Tetsu, additional

Published
2013
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36. Essential Role for CD30-Transglutaminase 2 Axis in Memory Th1 and Th17 Cell Generation

Author

Akane S. Suzuki, Ryoji Yagi, Motoko Y. Kimura, Chiaki Iwamura, Kenta Shinoda, Atsushi Onodera, Kiyoshi Hirahara, Damon J. Tumes, Ryo Koyama-Nasu, Siiri E. Iismaa, Robert M. Graham, Shinichiro Motohashi, Toshinori Nakayama, Suzuki, Akane S, Yagi, Ryoji, Kimura, Motoko Y, Iwamura, Chiaki, Shinoda, Kenta, Onodera, Atsushi, Hirahara, Kiyoshi, Tumes, Damon J, Koyama-Nasu, Ryo, Iismaa, Siiri E, Graham, Robert M, Motohashi, Shinichiro, and Nakayama, Toshinori

Subjects
0301 basic medicine, lcsh:Immunologic diseases. Allergy, CD30, Tissue transglutaminase, Immunology, Ki-1 Antigen, Cell generation, Mice, Transgenic, airway inflammation, Immunophenotyping, Pathogenesis, memory Th cell generation, Th1, Mice, 03 medical and health sciences, 0302 clinical medicine, Immune system, TG2, GTP-Binding Proteins, Animals, Immunology and Allergy, Protein Glutamine gamma Glutamyltransferase 2, Original Research, Transglutaminases, biology, Chemistry, Effector, memory precursor, Airway inflammation, Cell Differentiation, Th1 Cells, Adoptive Transfer, Cell biology, Antibody production, 030104 developmental biology, biology.protein, Th17 Cells, Th17, lcsh:RC581-607, Immunologic Memory, Signal Transduction, 030215 immunology
Abstract

Memory helper T (Th) cells are crucial for secondary immune responses against infectious microorganisms but also drive the pathogenesis of chronic inflammatory diseases. Therefore, it is of fundamental importance to understand how memory T cells are generated. However, the molecular mechanisms governing memory Th cell generation remain incompletely understood. Here, we identified CD30 as a molecule heterogeneously expressed on effector Th1 and Th17 cells, and CD30(hi)effector Th1 and Th17 cells preferentially generated memory Th1 and Th17 cells. We found that CD30 mediated signal induced Transglutaminase-2 (TG2) expression, and that the TG2 expression in effector Th cells is essential for memory Th cell generation. In fact,Cd30-deficiency resulted in the impaired generation of memory Th1 and Th17 cells, which can be rescued by overexpression of TG2. Furthermore, transglutaminase-2(Tgm2)-deficient CD4 T cells failed to become memory Th cells. As a result, T cells fromTgm2-deficient mice displayed impaired antigen-specific antibody production and attenuated Th17-mediated allergic responses. Our data indicate that CD30-induced TG2 expression in effector Th cells is essential for the generation of memory Th1 and Th17 cells, and that CD30 can be a marker for precursors of memory Th1 and Th17 cells. Refereed/Peer-reviewed

Published
2020
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37. ACC1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis

Author

Takahiro Nakajima, Yusuke Endo, Hirotaka Kanuka, Kazushige Obata-Ninomiya, Kenji Ishiwata, Toshio Kanno, Toshinori Nakayama, Hikari K. Asou, Atsushi Onodera, Damon J. Tumes, Takeshi Yamamoto, Toshihiro Ito, Ryo Koyama-Nasu, Endo, Yusuke, Onodera, Atsushi, Obata-Ninomiya, Kazushige, Koyama-Nasu, Ryo, Asou, Hikari K, Ito, Toshihiro, Yamamoto, Takeshi, Kanno, Toshio, Nakajima, Takahiro, Ishiwata, Kenji, Kanuka, Hirotaka, Tumes, Damon J, and Nakayama, Toshinori

Subjects
ACACA, education.field_of_study, Fatty acid metabolism, Effector, Chemistry, Endocrinology, Diabetes and Metabolism, Population, Cell Biology, Cell fate determination, Acquired immune system, infection, Cell biology, immunological memory, chemistry.chemical_compound, medicine.anatomical_structure, Physiology (medical), Internal Medicine, medicine, education, Memory T cell, Gene, metabolism, CD4-positive T cells
Abstract

Immunological memory is central to adaptive immunity and protection from disease. Changing metabolic demands as antigen-specific T cells transition from effector to memory cells have been well documented, but the cell-specific pathways and molecules that govern this transition are poorly defined. Here we show that genetic deletion of ACC1, a rate-limiting enzyme in fatty acid biosynthesis, enhances the formation of CD4+ T memory cells. ACC1-deficient effector helper T (Th) cells have similar metabolic signatures to wild-type memory Th cells, and expression of the gene encoding ACC1, Acaca, was inversely correlated with a memory gene signature in individual cells. Inhibition of ACC1 function enhances memory T cell formation during parasite infection in mice. Using single-cell analyses we identify a memory precursor-enriched population (CCR7hiCD137lo) present during early differentiation of effector CD4+ T cells. Our data indicate that fatty acid metabolism directs cell fate determination during the generation of memory CD4+ T cells.

Published
2019

38. Role of F-box protein betaTrcp1 in mammary gland development and tumorigenesis.

Author

Kudo Y, Guardavaccaro D, Santamaria PG, Koyama-Nasu R, Latres E, Bronson R, Yamasaki L, and Pagano M

Subjects
Animals, Base Sequence, DNA genetics, Female, Gene Targeting, Humans, Mammary Glands, Animal abnormalities, Mammary Neoplasms, Experimental genetics, Mammary Neoplasms, Experimental pathology, Mice, Mice, Knockout, Mice, Transgenic, Phenotype, Recombinant Proteins genetics, Recombinant Proteins metabolism, beta-Transducin Repeat-Containing Proteins deficiency, beta-Transducin Repeat-Containing Proteins genetics, Mammary Glands, Animal growth & development, Mammary Neoplasms, Experimental etiology, beta-Transducin Repeat-Containing Proteins physiology
Abstract

The F-box protein betaTrcp1 controls the stability of several crucial regulators of proliferation and apoptosis, including certain inhibitors of the NF-kappaB family of transcription factors. Here we show that mammary glands of betaTrcp1(-/-) female mice display a hypoplastic phenotype, whereas no effects on cell proliferation are observed in other somatic cells. To investigate further the role of betaTrcp1 in mammary gland development, we generated transgenic mice expressing human betaTrcp1 targeted to epithelial cells under the control of the mouse mammary tumor virus (MMTV) long terminal repeat promoter. Compared to controls, MMTV betaTrcp1 mammary glands display an increase in lateral ductal branching and extensive arrays of alveolus-like protuberances. The mammary epithelia of MMTV betaTrcp1 mice proliferate more and show increased NF-kappaB DNA binding activity and higher levels of nuclear NF-kappaB p65/RelA. In addition, 38% of transgenic mice develop tumors, including mammary, ovarian, and uterine carcinomas. The targeting of betaTrcp1 to lymphoid organs produces no effects on these tissues. In summary, our results support the notion that betaTrcp1 positively controls the proliferation of breast epithelium and indicate that alteration of betaTrcp1 function and expression may contribute to malignant behavior of breast tumors, at least in part through NF-kappaB transactivation.

Published
2004
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