SATO Katsuaki

写真a

Affiliation

Faculty of Medicine School of Medicine Department of Infectious Diseases, Immunology

Title

Professor

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Degree 【 display / non-display

  • 博士(理学) ( 1996.3   北海道大学 )

Research Areas 【 display / non-display

  • Life Science / Immunology  / Immunology

 

Papers 【 display / non-display

  • Effect of Hepatic Lipid Overload on Accelerated Hepatocyte Proliferation Promoted by HGF Expression via the SphK1/S1PR2 Pathway in MCD-diet Mouse Partial Hepatectomy Reviewed

    2 ( 3 )   100087   2025.8

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:JAPAN SOCIETY OF HISTOCHEMISTRY AND CYTOCHEMISTRY  

    DOI: 10.1016/j.bneo.2025.100087

  • Selectivity of bovine interleukin-2 mutein stimulation on bovine peripheral blood mononuclear cells Reviewed

    MITOMA Shuya, UTO Tomofumi, FUKAYA Tomohiro, TOMINAGA Moe, SEKIGUCHI Satoshi, SATO Katsuaki, NORIMINE Junzo

    Journal of Veterinary Medical Science   87 ( 7 )   781 - 790   2025

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:JAPANESE SOCIETY OF VETERINARY SCIENCE  

    Delivery of engineered interleukin-2 (IL-2) variants (muteins) is thought to be a promising cancer therapy in humans and mice. Our previous study indicated that bovine IL-2 (boIL-2) has a great potential to elicit NK cell activity for which distribution of IL-2 receptors on the target cell surface influences signal transduction. We developed nine boIL-2 muteins and examined the influence of the muteins on bovine peripheral blood mononuclear cells <i>in vitro</i>. On bovine peripheral mononuclear cells, NK cells strongly expressed CD122, followed by CD8<sup>+</sup> T cells, while CD4<sup>+</sup> T cells and γδ T cells did not show significant CD122 expression. All boIL-2 muteins showed decreasing in binding to boIL-2 receptor α, CD25, while maintaining their ability to bind to boIL-2 receptor βγ, CD122/CD132, heterodimer. The mutein F44A and E63A suppressed CD4<sup>+</sup> T cell expansion but maintained the NK cell expansion. These results indicate that boIL-2 muteins can alter immunological outcomes and may be used for clinical intervention for a disease progression.

    DOI: 10.1292/jvms.24-0470

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  • Effect of Hepatic Lipid Overload on Accelerated Hepatocyte Proliferation Promoted by HGF Expression via the SphK1/S1PR2 Pathway in MCD-diet Mouse Partial Hepatectomy Reviewed

    Lkham-Erdene B, Choijookhuu N, Kubota T, Uto T, Mitoma S, Shirouzu S, Ishizuka T, Kai K, Higuchi K, Mo Aung K, Batmunkh JE, Sato K, Hishikawa Y

    Acta histochemica et cytochemica   57 ( 5 )   175 - 188   2024.10

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:日本組織細胞化学会  

    Metabolic dysfunction-associated steatotic liver disease (MASLD) is becoming a major health problem worldwide. Liver regeneration is crucial for restoring liver function, and is regulated by extraordinary complex process, involving numerous factors under both physiologic and pathologic conditions. Sphingosine-1-phosphate (S1P), a bioactive sphingolipid synthesized by sphingosine kinase 1 (SphK1), plays an important role in liver function through S1P receptors (S1PRs)-expressing cells. In this study, we investigated the effect of lipid overload on hepatocyte proliferation in a mouse hepatic steatosis model induced by feeding a methionine- and choline-deficient (MCD) diet. After 50% partial hepatectomy (PHx), liver tissues were sampled at various timepoints and then analyzed by immunohistochemistry, oil Red-O staining, quantitative-polymerase chain reaction (qPCR), and flow cytometry. In mice fed the MCD-diet, significantly exacerbated hepatic steatosis and accelerated liver regeneration were observed. After PHx, hepatocyte proliferation peaked at 48 and 36 hr in the liver of chow- and MCD-diet fed mice, respectively. By contrast, increased expression of S1PR2 was observed in hepatic neutrophils and macrophages of MCD-diet fed mice. Flow cytometry and qPCR experiments demonstrated that levels of HGF and FGF2 released by neutrophils and macrophages were significantly higher in MCD-diet fed mice. In conclusion, hepatic lipid overload recruits Kupffer cells and neutrophils that release HGF and FGF2 via SphK1/S1PR2 activation to accelerate hepatocyte proliferation.

    DOI: 10.1267/ahc.24-00046

    PubMed

    CiNii Research

  • Crucial role of dendritic cells in the generation of anti-tumor T-cell responses and immunogenic tumor microenvironment to suppress tumor development Reviewed International coauthorship

    Tominaga M, Uto T, Fukaya T, Mitoma S, Riethmacher D, Umekita K, Yamashita Y, Sato K

    Frontiers in immunology   15   1200461   2024

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.3389/fimmu.2024.1200461

    PubMed

  • Tmem161a regulates bone formation and bone strength through the P38 MAPK pathwayduring liver regeneration Reviewed

    Nagai, T., Sekimoto, T., Kurogi, S., Ohta, T., Miyazaki, S., Yamaguchi, Y.,84. Tajima, T., Chosa, E., Imasaka, M., Yoshinobu, K., Araki, K., Araki, M., Choijookhuu, N., Sato, K., Hishikawa, Y., and Funamoto T.

    Scientific Reports   13 ( 1 )   14639   2023.9

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41598-023-41837-4.

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Books 【 display / non-display

  • Current Topics in Microbiology and Immunology

    Sato, K. Uto, T., Fukaya, T., and Takagi, H.( Role: Joint author)

    Springer Publishing  2017.9 

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    Language:English Book type:Scholarly book

  • Chronic inflammation: Mechanisms and Regulation

    Sato, K.( Role: Sole author)

    Springer Publishing  2016.11 

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    Language:English Book type:Scholarly book

  • Methods in Molecular Biology

    Fukaya, T., Takagi, H., Uto, T, Arimura, K., and Sato, K.( Role: Joint author)

    Springer Publishing  2016.5 

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    Language:English Book type:Scholarly book

  • 臍帯血移植の基礎と臨床

    清野研一郎?佐藤克明( Role: Joint author)

    医学書院  2014.10 

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    Language:Japanese Book type:Scholarly book

MISC 【 display / non-display

  • 樹状細胞のはたらき⑧樹状細胞を標的とした免疫チェックポイント阻害療法 Invited

    宇都倫史•深谷知宏•三苫修也•佐藤克明

    Veterinary Immunology for Practitioners   37   26 - 31   2025.1

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    Authorship:Corresponding author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

  • 樹状細胞のはたらき⑦がん免疫応答における通常型樹状細胞の役割 Invited

    宇都倫史•深谷知宏•三苫修也•佐藤克明

    Veterinary Immunology for Practitioners   36   46 - 51   2024.10

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    Authorship:Corresponding author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

  • 樹状細胞のはたらき⑥アレルギー疾患に対する舌下免疫療法の防御効果における樹状細胞の役割 Invited

    深谷知宏•宇都倫史•三苫修也•佐藤克明

    Veterinary Immunology for Practitioners   35   44 - 49   2024.7

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    Authorship:Corresponding author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

  • 樹状細胞のはたらき⑤幼若期での抗生剤服用による消化管細菌叢異常に基づく経口免疫寛容の破綻における通常型樹状細胞の役割 Invited

    深谷知宏•宇都倫史•三苫修也•佐藤克明

    Veterinary Immunology for Practitioners   34   15 - 21   2024.4

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    Authorship:Corresponding author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

  • 樹状細胞のはたらき④経口免疫寛容の誘導における形質細胞様樹状細胞の役割 Invited

    深谷知宏•宇都倫史•三苫修也•佐藤克明

    Veterinary Immunology for Practitioners   33   15 - 19   2024.1

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    Authorship:Corresponding author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

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Presentations 【 display / non-display

  • Clec4A4 acts as a negative immune checkpoint regulator to suppress antitumor immunity

    宇都倫史、深谷知宏、三苫修也、佐藤克明

    第54回日本免疫学会学術集会  2025.12.10 

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    Event date: 2025.12.10 - 2025.12.12

    Language:English   Presentation type:Poster presentation  

  • Crucial role of dendritic cells in the generation of anti-tumor T-cell responses and immunogenic tumor microenvironment to suppress tumor development

    三苫修也、宇都倫史、深谷知宏、佐藤克明

    第54回日本免疫学会学術集会  2025.12.12 

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    Event date: 2025.12.10 - 2025.12.12

    Language:English   Presentation type:Poster presentation  

  • Gut dysbiosis drives the impairment of oral tolerance mediated through mucosal dendritic cell dysfunction

    深谷知宏、宇都倫史、三苫修也、佐藤克明

    第54回日本免疫学会学術集会  2025.12.12 

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    Event date: 2025.12.10 - 2025.12.12

    Language:English   Presentation type:Poster presentation  

  • 樹状細胞による免疫寛容の誘導に基づくアレルギー制御 Invited

    深谷知宏、佐藤克明

    日本食品免疫学会第21回学術大会  2025.10.2 

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    Event date: 2025.10.2

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

  • 新規樹状細胞発現免疫チェックポイント分子Clec4A4によるがん免疫制御機構

    宇都倫史、深谷知宏、三苫修也、佐藤克明

    第29回日本がん免疫学会総会  2025.7.26 

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    Event date: 2025.7.24 - 2025.7.26

    Language:Japanese   Presentation type:Oral presentation (general)  

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Awards 【 display / non-display

  • 平成28年度(第52回)宮崎日日新聞賞「科学賞」

    2016.10   宮崎日日新聞社  

    佐藤克明

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    Award type:Award from publisher, newspaper, foundation, etc.  Country:Japan

  • 平成27年度宮崎大学教員教育活動表彰者

    2015.9   国立大学法人宮崎大学  

    佐藤克明

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    Country:Japan

Grant-in-Aid for Scientific Research 【 display / non-display

  • 新規ヒト樹状細胞標的免疫チェックポイント阻害剤の創生

    Grant number:25K02533  2025.04 - 2028.03

    独立行政法人日本学術振興会  科学研究費基金  基盤研究(B)

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    Authorship:Principal investigator 

  • ヒト樹状細胞発現機能制御分子を標的とした新規免疫チェックポイント阻害剤の開発

    Grant number:23K24185  2024.04 - 2025.03

    独立行政法人日本学術振興会  科学研究費基金  基盤研究(B)

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    Authorship:Principal investigator 

  • 新規ヒト樹状細胞発現免疫チェックポイント分子を標的とした阻害剤の開発

    Grant number:23H02773  2023.04 - 2026.03

    科学研究費補助金  基盤研究(B)

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    Authorship:Coinvestigator(s) 

  • 形質細胞様樹状細胞の機能制御分子を標的とした新規免疫チェックポイント阻 害剤の開

    Grant number:23K06768  2023.04 - 2026.03

    科学研究費補助金  基盤研究(C)

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    Authorship:Coinvestigator(s) 

    形質細胞様樹状細胞による経口免疫寛容成立の制御機構の解明

  • ヒト樹状細胞発現機能制御分子を標的とした新規免疫チェックポイント阻害剤の開発

    Grant number:22H02924  2022.04 - 2025.03

    独立行政法人日本学術振興会  科学研究費補助金  基盤研究(B)

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    Authorship:Principal investigator 

    通常型樹状細胞のIL-22RA2による上皮組織恒常性維持に対する制御機構の解明

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Other research activities 【 display / non-display

  • 宮崎日日新聞

    2018.07

  • 読売新聞

    2018.02

  • 日本経済新聞朝刊

    2017.08

  • 薬事日報朝刊

    2016.12

  • BIGLOBEニュース

    2016.11

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