2022/09/29 更新

写真a

サイダ ユウ
才田 優
SAIDA Yu
所属
医歯学総合病院 呼吸器・感染症内科 助教
職名
助教
外部リンク

学位

  • 博士(医学) ( 2015年9月 )

研究キーワード

  • 肺癌

研究分野

  • ライフサイエンス / 腫瘍生物学

経歴(researchmap)

  • 新潟大学医歯学総合病院 呼吸器・感染症内科

    2021年4月 - 現在

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経歴

  • 新潟大学   医歯学総合病院 呼吸器・感染症内科   助教

    2021年4月 - 現在

学歴

  • 新潟大学   医学部医学科

    2001年4月 - 2007年3月

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所属学協会

 

論文

  • Multimodal molecular imaging detects early responses to immune checkpoint blockade

    2021年4月

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  • Efficacy of EGFR-TKIs with or without upfront brain radiotherapy for EGFR-mutant NSCLC patients with central nervous system metastases

    2019年11月

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  • Effect of Lymphodepletion on Donor T Cells and the Role of Recipient Cells Persisting after Cytotoxic Treatments in Cancer Immunotherapies. 国際誌

    Satoshi Watanabe, Masashi Arita, Miho Takahashi, Yu Saida, Toshiyuki Koya, Toshiaki Kikuchi

    Critical reviews in immunology   37 ( 1 )   59 - 73   2017年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    The effectiveness of lymphodepletion in antitumor immunity has been well established. Although recent studies have elucidated some of the broad mechanisms underlying the augmentation of antitumor immunity by lymphodepletion, such as increased availability of cytokines due to the elimination of cellular elements and improvement in tumor antigen presentation, the precise mechanisms remain unclear. Previous studies have focused on the enhancement of the functions of transferred antitumor CD8+ T cells after lymphodepletion. In this review, we discuss the important role of other immune cells in the effectiveness of lymphodepletion. Recent studies have demonstrated that lymphodepletion enhances not only transferred tumor-specific CD8+ T cells but also tumor-specific CD4+ T cells and polyclonal naïve T cells. Moreover, recipient immune cells, including CD8+ T cells, regulatory T cells, dendritic cells, and macrophages, are involved in the augmentation of antitumor effects by lymphodepletion. These host cells can survive lymphodepletive therapies and play a role in the development of antitumor immunity after lymphodepletion. Improvements in the understanding of lymphodepletion allow us to design effective cancer immunotherapy.

    DOI: 10.1615/CritRevImmunol.2018019497

    PubMed

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  • Transfer of in vitro-expanded naïve T cells after lymphodepletion enhances antitumor immunity through the induction of polyclonal antitumor effector T cells. 国際誌

    Tomohiro Tanaka, Satoshi Watanabe, Miho Takahashi, Ko Sato, Yu Saida, Junko Baba, Masashi Arita, Miyuki Sato, Aya Ohtsubo, Satoshi Shoji, Koichiro Nozaki, Kosuke Ichikawa, Rie Kondo, Nobumasa Aoki, Yasuyoshi Ohshima, Takuro Sakagami, Tetsuya Abe, Hiroshi Moro, Toshiyuki Koya, Junta Tanaka, Hiroshi Kagamu, Hirohisa Yoshizawa, Toshiaki Kikuchi

    PloS one   12 ( 8 )   e0183976   2017年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    The adoptive transfer of effector T cells combined with lymphodepletion has demonstrated promising antitumor effects in mice and humans, although the availability of tumor-specific T cells is limited. We and others have also demonstrated that the transfer of polyclonal naïve T cells induces tumor-specific effector T cells and enhances antitumor immunity after lymphodepletion. Because tumors have been demonstrated to induce immunosuppressive networks and regulate the function of T cells, obtaining a sufficient number of fully functional naïve T cells that are able to differentiate into tumor-specific effector T cells remains difficult. To establish culture methods to obtain a large number of polyclonal T cells that are capable of differentiating into tumor-specific effector T cells, naïve T cells were activated with anti-CD3 mAbs in vitro. These cells were stimulated with IL-2 and IL-7 for the CD8 subset or with IL-7 and IL-23 for the CD4 subset. Transfer of these hyperexpanded T cells after lymphodepletion showed significant antitumor efficacy, and tumor-specific effector T cells were primed from these expanded T cells in tumor-bearing hosts. Moreover, these ex vivo-expanded T cells maintained T cell receptor diversity and showed long-term persistence of memory against specific tumors. Further analyses revealed that combination therapy consisting of vaccination with dendritic cells that were co-cultured with irradiated whole tumor cells and the transfer of ex vivo-expanded T cells significantly enhanced antitumor immunity. These results indicate that the transfer of ex vivo-expanded polyclonal T cells can be combined with other immunotherapies and augment antitumor effects.

    DOI: 10.1371/journal.pone.0183976

    PubMed

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  • Critical roles of chemo-resistant effector and regulatory T cells in antitumor immunity after lymphodepleting chemotherapy

    2015年7月

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  • Recurrent Interstitial Lung Disease Induced By Various Therapies for Non-Small Cell Lung Cancer. J Clin Case Rep

    2014年12月

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  • Depletion of radio-resistant regulatory T cells enhances antitumor immunity during recovery from lymphopenia. 国際誌

    Junko Baba, Satoshi Watanabe, Yu Saida, Tomohiro Tanaka, Takao Miyabayashi, Jun Koshio, Kosuke Ichikawa, Koichiro Nozaki, Toshiyuki Koya, Katsuya Deguchi, Chunrui Tan, Satoru Miura, Hiroshi Tanaka, Junta Tanaka, Hiroshi Kagamu, Hirohisa Yoshizawa, Ko Nakata, Ichiei Narita

    Blood   120 ( 12 )   2417 - 27   2012年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Cytotoxic lymphodepletion therapies augment antitumor immune responses. The generation and therapeutic efficacy of antitumor effector T cells (T(E)s) are enhanced during recovery from lymphopenia. Although the effects of lymphodepletion on naive T cells (T(N)s) and T(E)s have been studied extensively, the influence of lymphodepletion on suppressor cells remains poorly understood. In this study, we demonstrate a significant increase of CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) in sublethally irradiated lymphopenic mice. These radio-resistant Tregs inhibited the induction of T(E)s in tumor-draining lymph-nodes (TDLNs) during recovery from lymphopenia. The transfer of T(N)s into lymphopenic tumor-bearing mice resulted in some antitumor effects; however, Treg depletion after whole-body irradiation and reconstitution strongly inhibited tumor progression. Further analyses revealed that tumor-specific T cells were primed from the transferred T(N)s, whereas the Tregs originated from irradiated recipient cells. As in irradiated lymphopenic mice, a high percentage of Tregs was observed in cyclophosphamide-treated lymphopenic mice. The inhibition of Tregs in cyclophosphamide-treated mice significantly reduced tumor growth. These results indicate that the Tregs that survive cytotoxic therapies suppress antitumor immunity during recovery from lymphopenia and suggest that approaches to deplete radio and chemo-resistant Tregs can enhance cancer immunotherapies.

    PubMed

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  • Case of IgG4-related tubulointerstitial nephritis showing the progression of renal dysfunction after a cure for autoimmune pancreatitis.

    2010年

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