Details of the Researcher

PHOTO

Shunichi Tayama
Section
Graduate School of Medicine
Job title
Assistant Professor
Degree

  • PhD (Medicine) (Tohoku University)

e-Rad No.
80980416

Research History 4

  • 2023/04 - Present
    Tohoku University　Graduate School of Medicine　Assistant professor

  • 2020/04 - 2023/03
    Tohoku University

  • 2020/04 - 2023/03
    Japan Society for the Promotion of Science DC1

  • 2018/04 - 2019/03
    Tohoku University

Education 3

  • Tohoku University　Graduate School of Medicine

    2019/04 - 2023/03

  • Tohoku University　Graduate School of Medicine

    2017/04 - 2019/03

  • Tohoku university　Faculty of Science　Department of Biology

    2013/04 - 2017

Professional Memberships 2

  • American Association of Immunologists

  • 日本免疫学会

Research Interests 3

  • 炎症性疾患

  • 活性イオウ代謝

  • T細胞

Research Areas 1

  • Life sciences / Immunology /

Awards 10

  1. 医学奨励賞

    2026/01　宮城県医師会

  2. 坂田賞

    2026/01　東北大学 医学部

  3. 医学部奨学賞 銀賞

    2026/01　東北大学医学部

  4. Tadamitsu Kishimoto International Award

    2023/03　日本免疫学会

  5. AAI Trainee Abstract Award

    2023/03　American Association of Immunologists

  6. Young Investigator Award

    2022/10　The 12th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide

  7. ブースター研究奨励賞 最優秀賞

    2020/10　東北大学大学院医学系研究科

  8. Tadamitsu Kishimoto International Award

    2020/03　日本免疫学会

  9. AAI Trainee Abstract Award

    2020/02

  10. スターター研究奨励賞

    2019/10　東北大学大学院医学系研究科

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Papers 12

  1. Circulating memory-phenotype CD4+ T cells rapidly accumulate in the ischemic gut to exacerbate tissue injury in an innate manner Peer-reviewed

    Kosuke Sato, Shunichi Tayama, Akihisa Kawajiri, Jing Li, Ziying Yang, Ryoji Mitsuwaka, Feng Gao, Natsuki Asami, Reoka Aoki, Hiroyuki Nagashima, Kenshiro Matsuda, Chigusa Nakahashi-Oda, Yoichiro Iwakura, Akira Shibuya, Motoshi Wada, Naoto Ishii, Takeshi Kawabe

    Cell Reports　45　(8)　117745-117745　2026/08

    Publisher: Elsevier BV

    DOI： 10.1016/j.celrep.2026.117745 　

    ISSN： 2211-1247

  2. Supersulfide controls intestinal inflammation by suppressing CD4+ T cell proliferation Peer-reviewed

    Shunichi Tayama, Yuya Kitamura, Kyoga Hiraide, Hibiki Suzuki, Jing Li, Ziying Yang, Ryoji Mitsuwaka, Akihisa Kawajiri, Kosuke Sato, Feng Gao, Taku Nakai, Yuko Okuyama, Tadahisa Numakura, Mitsuhiro Yamada, Tomoaki Ida, Masanobu Morita, Takeshi Kawabe, Takaaki Akaike, Naoto Ishii

    Frontiers in Immunology　16　2025/04/15

    Publisher: Frontiers Media SA

    DOI： 10.3389/fimmu.2025.1506580 　

    eISSN： 1664-3224

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    Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation where CD4+ T lymphocytes play an essential role. Accumulating evidence suggests that immune responses driven by CD4+ T cells are critically regulated by various metabolic pathways including oxidative phosphorylation and glycolysis. Here we show that CARS2/CPERS-dependent supersulfide metabolism restrains CD4+ T cell proliferation in a cell-intrinsic manner. Under steady state, Cars2+/- mice exhibited spontaneous accumulation of effector/memory CD4+ T cells in the colon with age. In lymphopenic conditions, Cars2+/- CD4+ T cells showed enhanced cell cycle entry with reduced expression of a cell cycle inhibitor Trp53 and triggered an exacerbated form of colitis, the response being rescued by treatment with a supersulfide donor glutathione trisulfide (GSSSG). Furthermore, re-analysis of publicly available gene datasets of human colonic CD4+ T lymphocytes revealed that downregulation of CARS2 was associated with pathogenesis of IBD, and indeed, addition of GSSSG inhibited human CD4+ T cell proliferation in vitro. Together these observations reveal that CARS2/CPERS-dependent supersulfide metabolism is essential for homeostasis of intestinal effector/memory CD4+ T cells, and further suggest that dysregulation of the same metabolic pathway can lead to development of gut inflammation both in mice and humans.

  3. Naturally arising memory-phenotype CD4+ T lymphocytes give rise to multiple helper subsets to contribute to tumor immunity while inhibiting GVHD Peer-reviewed

    Ziying Yang, Jing Li, Hideaki Watanabe, Feng Gao, Akihisa Kawajiri, Keita Koinuma, Kosuke Sato, Yuko Okuyama, Shunichi Tayama, Yoichiro Iwakura, Naoto Ishii, Takeshi Kawabe

    Cancer Immunology Research　2025/04/01

    Publisher: American Association for Cancer Research (AACR)

    DOI： 10.1158/2326-6066.cir-24-0598 　

    ISSN： 2326-6066

    eISSN： 2326-6074

    More details Close

    Abstract Memory-phenotype (MP) CD4+ T lymphocytes spontaneously develop in steady state from peripheral naïve precursors in a manner dependent on self-antigen recognition. While MP cells possess innate type 1 and 3 effector functions that can contribute to host defense and autoimmunity, their immunological functions in tumor immunity and graft-versus-host disease (GVHD), which results from therapeutic bone marrow transplantation (BMT) against hematological malignancies, remain unclear. Here we show that in mixed lymphocyte reactions, MP lymphocytes can generate T helper 1 (Th1), T helper 17 (Th17), and regulatory T (Treg) cell subsets, whereas naïve cells dominantly differentiate to Th1. Consistent with this, naïve lymphocytes mainly induce Th1 responses in the mouse EL4 model of malignant lymphoma and the B16 model of malignant melanoma, whereas MP cells efficiently give rise to Th1, Th17, and Treg subsets to exert mild, IFN--dependent antitumor activities in vivo. Moreover, we demonstrate using a mouse model of BMT that MP cells more efficiently differentiate into Treg cells to partially suppress GVHD as compared to naïve T lymphocytes. Furthermore, our data suggest that when used as donor T lymphocytes in BMT in tumor-bearing mice, MP cells give rise to Th1, Th17, and Treg cells to generate antitumor responses without inducing GVHD. Together these results identify MP cells as a unique T-cell population that has potential to generate multiple T helper subsets including Th1 and Treg cells, thereby contributing to tumor immunity while inhibiting development of BMT-associated GVHD.

  4. Naturally arising memory-phenotype CD4 + T lymphocytes contain an undifferentiated population that can generate T H 1, T H 17, and T reg cells Peer-reviewed

    Akihisa Kawajiri, Jing Li, Keita Koinuma, Ziying Yang, Hye Jin Yoon, Jaeu Yi, Hiroyuki Nagashima, Minami Ishii, Feng Gao, Kosuke Sato, Shunichi Tayama, Hideo Harigae, Yoichiro Iwakura, Naoto Ishii, Alan Sher, Kazuyoshi Ishigaki, Jinfang Zhu, Kwang Soon Kim, Takeshi Kawabe

    Science Advances　10　(49)　2024/12/06

    Publisher: American Association for the Advancement of Science (AAAS)

    DOI： 10.1126/sciadv.adq6618 　

    eISSN： 2375-2548

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    Memory-phenotype (MP) CD4 + T lymphocytes develop from naïve cells via self-recognition at homeostasis. While previous studies defined MP cells as a heterogeneous population that comprises T helper 1 (T H 1)/17–like subsets, functional significance of the T-bet − Rorγt − subpopulation remains unknown. Here we show that MP lymphocytes as a whole population can differentiate into T H 1/17/regulatory T (T reg ) cells to mediate mild and persistent inflammation in lymphopenic environments, whereas naïve cells exhibit strong, T H 1-dominated responses. Moreover, we demonstrate that MP lymphocytes comprise not only T H 1/17-differentiated subsets but a polyclonal, transcriptomically immature “undifferentiated” subpopulation at homeostasis. Furthermore, our data argue that while the T-bet + Rorγt − MP subset is terminally T H 1-differentiated, its undifferentiated counterpart retains the capacity to rapidly proliferate to differentiate into T H 1/17/T reg cells, with the latter response tonically constrained by preexisting T reg cells. Together, our results identify undifferentiated MP CD4 + T lymphocytes as a unique precursor that has a diverse differentiation potential to generate T H 1/17/T reg cells to contribute to pathogenesis of inflammation.

  5. Excess generation and activation of naturally arising memory-phenotype CD4+ T lymphocytes are inhibited by regulatory T cells in steady state Peer-reviewed

    Jing Li, Ziying Yang, Akihisa Kawajiri, Kosuke Sato, Shunichi Tayama, Naoto Ishii, Jinfang Zhu, Takeshi Kawabe

    Frontiers in Immunology　15　2024/08/16

    Publisher: Frontiers Media SA

    DOI： 10.3389/fimmu.2024.1429954 　

    eISSN： 1664-3224

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    Conventional CD4+ T lymphocytes consist of naïve, foreign antigen-specific memory, and self-antigen-driven memory-phenotype (MP) cell compartments at homeostasis. We recently showed that MP cells tonically proliferate in response to self-antigens and differentiate into the T-bet+ subset in steady state. How excess proliferation and differentiation of MP cells are inhibited remains unclear. Given immunosuppressive function of regulatory T cells (Tregs), it is possible that they are also involved in inhibition of spontaneous MP cell activation. Here we show using Foxp3-diphtheria toxin receptor-transgenic mice that both MP and naïve CD4+ T cells spontaneously proliferate and differentiate into Th1 cells upon acute Treg depletion. At an early time point post Treg depletion, MP as compared to naïve CD4+ T cells are preferentially activated while at a later stage, the response is dominated by activated cells originated from the naïve pool. Moreover, we argue that MP cell proliferation is driven by TCR and CD28 signaling whereas Th1 differentiation mediated by IL-2. Furthermore, our data indicate that such activation of MP and naïve CD4+ T lymphocytes contribute to development of multi-organ inflammation at early and later time points, respectively, after Treg ablation. Together our findings reveal that Tregs tonically inhibit early, spontaneous proliferation and Th1 differentiation of MP CD4+ T lymphocytes as well as late activation of naïve cells, thereby contributing to maintenance of T cell homeostasis.

  6. Glutathione supersulphide regulates T-cell receptor signalling

    Yusaku Sasaki, Tadahisa Numakura, Mitsuhiro Yamada, Hisatoshi Sugiura, Tetsuro Matsunaga, Tomoaki Ida, Masanobu Morita, Ayumi Suzuki, Shuichiro Matsumoto, Madoka Kawaguchi, Takeshi Kawabe, Shunichi Tayama, Yuko Okuyama, Tsuyoshi Takata, Kenji Inaba, Satoshi Watanabe, Manami Suzuki, Hirohito Sano, Yorihiko Kyogoku, Rie Tanaka, Ayumi Mitsune, Tomohiro Ichikawa, Naoya Fujino, Tsutomu Tamada, Naoto Ishii, Masakazu Ichinose, Takaaki Akaike, Hozumi Motohashi

    bioRxiv : the preprint server for biology　2024/05/02

    Publisher: openRxiv

    DOI： 10.1101/2024.04.30.591985 　

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    Abstract Immunometabolism regulates functions and fates of immune cells including T cells. Supersulphides, which are universal metabolites containing catenated sulphur atoms, have various physiological functions based on their unique redox properties. Here we found that activation of T-cell receptor (TCR) signalling was accompanied by supersulphide decrease, which suggests a regulatory contribution of sulphur metabolism to immune function. Consistently, inhibiting supersulphide synthesis facilitated TCR activation and exacerbated allergen-induced type 2 inflammation in mice. Supplementation with glutathione trisulphide (GSSSG), a major endogenous supersulphide, suppressed TCR signalling in naïve CD4 + T cells and their differentiation and effectively alleviated the inflammation. Docking simulation revealed interaction of GSSSG with CD3ε chain in the TCR/CD3 complex, which was supported by mass spectrometry detection of persulphidated glutathionylation at a functionally important CXXC motif of CD3ε chain. This study identified a new post-translational modification with supersulfides and demonstrated a critical contribution of sulphur metabolism to TCR signalling regulation.

  7. Redefining the Foreign Antigen and Self-Driven Memory CD4+ T-Cell Compartments via Transcriptomic, Phenotypic, and Functional Analyses. International-journal Peer-reviewed

    Takeshi Kawabe, Thomas Ciucci, Kwang Soon Kim, Shunichi Tayama, Akihisa Kawajiri, Takumi Suzuki, Riou Tanaka, Naoto Ishii, Dragana Jankovic, Jinfang Zhu, Jonathan Sprent, Rémy Bosselut, Alan Sher

    Frontiers in immunology　13　870542-870542　2022

    DOI： 10.3389/fimmu.2022.870542 　

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    Under steady-state conditions, conventional CD4+ T lymphocytes are classically divided into naïve (CD44lo CD62Lhi) and memory (CD44hi CD62Llo) cell compartments. While the latter population is presumed to comprise a mixture of distinct subpopulations of explicit foreign antigen (Ag)-specific "authentic" memory and foreign Ag-independent memory-phenotype (MP) cells, phenotypic markers differentially expressed in these two cell types have yet to be identified. Moreover, while MP cells themselves have been previously described as heterogeneous, it is unknown whether they consist of distinct subsets defined by marker expression. In this study, we demonstrate using combined single-cell RNA sequencing and flow cytometric approaches that self-driven MP CD4+ T lymphocytes are divided into CD127hi Sca1lo, CD127hi Sca1hi, CD127lo Sca1hi, and CD127lo Sca1lo subpopulations that are Bcl2lo, while foreign Ag-specific memory cells are CD127hi Sca1hi Bcl2hi. We further show that among the four MP subsets, CD127hi Sca1hi lymphocytes represent the most mature and cell division-experienced subpopulation derived from peripheral naïve precursors. Finally, we provide evidence arguing that this MP subpopulation exerts the highest responsiveness to Th1-differentiating cytokines and can induce colitis. Together, our findings define MP CD4+ T lymphocytes as a unique, self-driven population consisting of distinct subsets that differ from conventional foreign Ag-specific memory cells in marker expression and establish functional relevance for the mature subset of CD127hi Sca1hi MP cells.

  8. Fatty acid-binding protein 3 regulates differentiation of IgM-producing plasma cells. International-journal Peer-reviewed

    Shuhei Kobayashi, Hai The Phung, Shunichi Tayama, Yoshiteru Kagawa, Hirofumi Miyazaki, Yui Yamamoto, Takashi Maruyama, Naoto Ishii, Yuji Owada

    The FEBS journal　288　(4)　1130-1141　2021/02

    DOI： 10.1111/febs.15460 　

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    Plasma cells (PCs), which aim to protect host health, produce various subsets of immunoglobulin (Ig) in response to extracellular pathogens. Blimp-1 (encoded by Prdm1)-a protein that is highly expressed by PCs-is important for PC functions, including the generation of Igs. Fatty acid-binding protein 3 (FABP3) is a carrier protein of polyunsaturated fatty acids (PUFAs) and participates in multiple cellular functions. Although the functions of FABP3 in neurons and cardiac myocytes are well-noted, their roles in immune cells remain to be fully elucidated. In this study, we demonstrate that FABP3 is expressed in activated B cells and that FABP3 promotes PC development and IgM secretion. Moreover, we provide the first evidence that FABP3 is necessary for Blimp-1 expression, by regulating the histone modification of its promoter region. Taken together, our findings reveal that FABP3 acts as a positive regulator of B-cell activation by controlling histone acetylation of the Blimp-1 gene, thereby playing a role in host defense against pathogens.

  9. Fatty acid-binding protein 5 limits ILC2-mediated allergic lung inflammation in a murine asthma model. International-journal Peer-reviewed

    Shuhei Kobayashi*, Shunichi Tayama*, Hai The Phung, Yoshiteru Kagawa, Hirofumi Miyazaki, Yu Takahashi, Takashi Maruyama, Naoto Ishii, Yuji Owada (*co-first author)

    Scientific reports　10　(1)　16617-16617　2020/10/06

    DOI： 10.1038/s41598-020-73935-y 　

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    Dietary obesity is regarded as a problem worldwide, and it has been revealed the strong linkage between obesity and allergic inflammation. Fatty acid-binding protein 5 (FABP5) is expressed in lung cells, such as alveolar epithelial cells (ECs) and alveolar macrophages, and plays an important role in infectious lung inflammation. However, we do not know precise mechanisms on how lipid metabolic change in the lung affects allergic lung inflammation. In this study, we showed that Fabp5-/- mice exhibited a severe symptom of allergic lung inflammation. We sought to examine the role of FABP5 in the allergic lung inflammation and demonstrated that the expression of FABP5 acts as a novel positive regulator of ST2 expression in alveolar ECs to generate retinoic acid (RA) and supports the synthesis of RA from type II alveolar ECs to suppress excessive activation of innate lymphoid cell (ILC) 2 during allergic lung inflammation. Furthermore, high-fat diet (HFD)-fed mice exhibit the downregulation of FABP5 and ST2 expression in the lung tissue compared with normal diet (ND)-fed mice. These phenomena might be the reason why obese people are more susceptible to allergic lung inflammation. Thus, FABP5 is potentially a therapeutic target for treating ILC2-mediated allergic lung inflammation.

  10. Correction: TRAF5 Deficiency Ameliorates the Severity of Dextran Sulfate Sodium Colitis by Decreasing TRAF2 Expression in Nonhematopoietic Cells. International-journal Peer-reviewed

    Hai The Phung, Hiroyuki Nagashima, Shuhei Kobayashi, Naoki Asano, Tomoaki Machiyama, Tsuyoshi Sakurai, Shunichi Tayama, Atsuko Asao, Akira Imatani, Takeshi Kawabe, Yuko Okuyama, Naoto Ishii, Takanori So

    ImmunoHorizons　4　(4)　216-216　2020/04/23

    DOI： 10.4049/immunohorizons.2000022 　

  11. IQ motif-containing GTPase-activating protein 1 is essential for the optimal maintenance of lung ILC2s. International-journal Peer-reviewed

    Shunichi Tayama, Yuko Okuyama, Hai The Phung, Atsuko Asao, Shuhei Kobayashi, Tomomi Musha, Tomoaki Machiyama, Tsuyoshi Sakurai, Chengming Zhang, Masuko Ushio-Fukai, Takeshi Kawabe, Takanori So, Naoto Ishii

    International immunology　32　(4)　233-241　2020/04/12

    DOI： 10.1093/intimm/dxz077 　

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    Group 2 innate lymphoid cells (ILC2s) play critical roles in type 2 immunity and are crucial for pathogenesis of various types of inflammatory disease. IQ motif-containing GTPase-activating protein 1 (IQGAP1) is a ubiquitously expressed scaffold protein that is involved in multiple cellular functions such as cell survival and trafficking. While the roles for IQGAP1 in T and B lymphocytes have been uncovered, the physiological significance of IQGAP1 in innate lymphocytes remains to be elucidated. In the current study, we demonstrate that using bone marrow chimeras, the deficiency of IQGAP1 caused an impaired survival of lung ILC2s in a cell-intrinsic manner and that Iqgap1-/- mice displayed decreased accumulation of ILC2s after administration of papain and thereby reduced the pathology of the disease. Moreover, Iqgap1-/- ILC2s showed a significantly enhanced apoptosis as compared to wild-type ILC2s under both steady-state and inflammatory conditions. Together these results identify for the first time that IQGAP1 is essential for homeostasis of ILC2s in the lung.

  12. TRAF5 Deficiency Ameliorates the Severity of Dextran Sulfate Sodium Colitis by Decreasing TRAF2 Expression in Nonhematopoietic Cells. International-journal Peer-reviewed

    Hai The Phung, Hiroyuki Nagashima, Shuhei Kobayashi, Naoki Asano, Tomoaki Machiyama, Tsuyoshi Sakurai, Shunichi Tayama, Atsuko Asao, Akira Imatani, Takeshi Kawabe, Yuko Okuyama, Naoto Ishii, Takanori So

    ImmunoHorizons　4　(3)　129-139　2020/03/10

    DOI： 10.4049/immunohorizons.2000007 　

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    TNFR-associated factor 5 (TRAF5) is a cytosolic adaptor protein and functions as an inflammatory regulator. However, the in vivo function of TRAF5 remains unclear, and how TRAF5 controls inflammatory responses in the intestine is not well understood. In this study, we found that intestinal epithelial cells from Traf5-/- mice expressed a significantly lower level of NF-κB-regulated proinflammatory genes, such as Tnf, Il6, and Cxcl1, as early as day 3 after dextran sulfate sodium (DSS) exposure when compared with wild-type mice. The intestinal barrier integrity of DSS-treated Traf5-/- mice remained intact at this early time point, and Traf5-/- mice showed decreased body weight loss and longer colon length at later time points. Surprisingly, the protein level of TRAF2, but not TRAF3, was reduced in colon tissues of Traf5-/- mice after DSS, indicating the requirement of TRAF5 for TRAF2 protein stability in the inflamed colon. Experiments with bone marrow chimeras confirmed that TRAF5 deficiency in nonhematopoietic cells caused the attenuated colitis. Our in vitro experiments demonstrated that proinflammatory cytokines significantly promoted the degradation of TRAF2 protein in Traf5-/- nonhematopoietic cells in a proteasome-dependent manner. Collectively, our data suggest a novel regulatory function of TRAF5 in supporting the proinflammatory function of TRAF2 in nonhematopoietic cells, which may be important for acute inflammatory responses in the intestine.

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Misc. 3

  1. Reactive persulfide controls intestinal inflammation by suppressing CD4+T cell proliferation

    Shunichi Tayama, Yuya Kitamura, Kyoga Hiraide, Jing Li, Ziying Yang, Akihisa Kawajiri, Kosuke Sato, Yuko Okuyama, Takeshi Kawabe, Takaaki Akaike, Naoto Ishii

    201　(S1)　61.01　2023

  2. 2型自然リンパ球における足場蛋白質IQGAP1の新たな役割 Invited Peer-reviewed

    田山舜一, 河部剛史, 石井直人

    臨床免疫・アレルギー科　74　(3)　226-233　2020/09

  3. IQ motif-containing GTPase-activating protein 1 is essential for the optimal maintenance of lung ILC2s

    Tayama S, Okuyama Y, Phung HT, Asao A, Kobayashi S, Kawabe T, So T, Ishii N

    204　(S1)　147.4　2020

Presentations 35

  1. Supersulfide Metabolism as a Therapeutic Target for T cell-mediated Inflammation Invited

    Shunichi Tayama

    UW–TU Engineering Medicine Kickoff Workshop　2026/03/27

  2. CARS2-dependent supersulfide metabolism exacerbates mouse model of multiple sclerosis by enhancing IFN-γ+ Th17 accumulation via promoting Il23p19 expression in dendritic cells

    Ryoji Mitsuwaka, Yuya Kitamura, Kyoga Hiraide, Hibiki Suzuki, Shunichi Tayama, Jing Li, Ziying Yang, Kosuke Sato, Yuko Okuyama, Takeshi Kawabe, Takaaki Akaike, Naoto Ishii

    The 54th Annual Meeting of The Japanese Society for Immunology　2025/12/11

  3. 多発性硬化症における超硫黄代謝の役割解明

    光若良治, 田山舜一, 鈴木響, 平出恭我, 北村祐哉, 河部剛史, 赤池孝章, 石井直人

    第77回 日本細菌学会東北支部 総会・学術集会　2025/08/22

  4. T細胞における超硫黄代謝の役割

    田山舜一

    第12回 若手研究者のためのネットワーキング　2025/06/02

  5. 大豆由来活性イオウ分子による大腸炎抑制機構の解明 Invited

    田山舜一, 河部剛史, 赤池孝章, 石井直人

    不二たん白財団・第28回研究報告会　2025/05/26

  6. Supersulfide controls intestinal inflammation by suppressing CD4+ T cell proliferation

    Shunichi Tayama, Yuya Kitamura, Kyoga Hiraide, Hibiki Suzuki, Jing Li, Ziying Yang, Ryoji Mitsuwaka, Akihisa Kawajiri, Kosuke Sato, Taku Nakai, Yuko Okuyama, Tadahisa Numakura, Mitsuhiro Yamada, Tomoaki Ida, Masanobu Morita, Takeshi Kawabe, Takaaki Akaike, Naoto Ishii

    Redox Week in Sendai 2025　2025/04/20

  7. 超硫黄代謝によるT細胞依存的炎症性腸疾患の制御 Invited

    田山舜一, 河部剛史, 赤池孝章, 石井直人

    第8回先進医薬研究報告会　2024/12/06

  8. Reactive persulfide controls intestinal inflammation by suppressing CD4+ T lymphocyte proliferation

    Shunichi Tayama, Yuya Kitamura, Kyoga Hiraide, Hibiki Suzuki, Jing Li, Ziying Yang, Kosuke Sato, Akihisa Kawajiri, Yuko Okuyama, Takeshi Kawabe, Takaaki Akaike, Naoto Ishii

    The 53rd Annual Meeting of The Japanese Society for Immunology　2024/12/03

  9. Mitochondrial cysteinyl-tRNA synthetase (CARS2) -dependent sulfur metabolism exacerbates a mouse model of multiple sclerosis through antigen presentation

    Hibiki Suzuki, Kyoga Hiraide, Yuya Kitamura, Shunichi Tayama, Kosuke Sato, Keita Koinuma, Yuko Okuyama, Takeshi Kawabe, Takaaki Akaike, Naoto Ishii

    The 52nd Annual Meeting of The Japanese Society for Immunology　2024/01/19

  10. Reactive persulfide controls intestinal inflammation by suppressing CD4+ T cell proliferation

    Shunichi Tayama, Yuya Kitamura, Kyoga Hiraide, Hibiki Suzuki, Jing Li, Ziying Yang, Kosuke Sato, Akihisa Kawajiri, Yuko Okuyama, Takeshi Kawabe, Takaaki Akaike, Naoto Ishii

    The 52nd Annual Meeting of The Japanese Society for Immunology　2024/01/18

  11. 新規活性イオウに代謝による実験的自己免疫性脳脊髄炎の発症制御

    鈴木響, 北村祐哉, 平出恭我, 田山舜一, 佐藤皓祐, 奥山祐子, 河部剛史, 赤池孝章, 石井直人

    第75回日本細菌学会東北支部総会・学術集会　2023/08/22

  12. 活性イオウ代謝によるT細胞機能制御機構の解明

    田山舜一, 北村祐哉, 平出恭我, 鈴木響, 李静, 楊子嬰, 川尻昭寿, 佐藤皓祐, 奥山祐子, 河部剛史, 赤池孝章, 石井直人

    第75回日本細菌学会東北支部総会・学術集会　2023/08/21

  13. Reactive persulfide controls intestinal inflammation by suppressing CD4+ T cell proliferation

    Shunichi Tayama, Yuya Kitamura, Kyoga Hiraide, Jing Li, Ziying Yang, Akihisa Kawajiri, Kosuke Sato, Yuko Okuyama, Takeshi Kawabe, Takaaki Akaike, Naoto Ishii

    Immunology 2023　2023/05/13

  14. T細胞における活性イオウの機能解明

    田山舜一

    第13回博士研究教育院生 研究成果発表会　2023/03/02

  15. 大腸炎惹起性CD4+ T細胞における活性イオウの機能解明

    田山舜一

    第16回リトリート大学院生研究発表会　2023/02/26

  16. Mitochondrial cysteinyl-tRNA synthetase (CARS2)-dependent sulfur metabolism exacerbates experimental autoimmune encephalomyelitis in mice

    Kyoga Hiraide, Yuya Kitamura, Shunichi Tayama, Yuko Okuyama, Kosuke Sato, Hibiki Suzuki, Keita Koinuma, Takeshi Kawabe, Naoto Ishii

    2022/12/07

  17. CARS2-dependent sulfur metabolism controls intestinal inflammation by suppressing CD4+ T cell proliferation

    Shunichi Tayama, Takeshi Kawabe, Yuya Kitamura, Kyoga Hiraide, Jing Li, Ziying Yang, Akihisa Kawajiri, Kosuke Sato, Yuko Okuyama, Naoto Ishii

    2022/12/07

  18. Persulfide controls T cell response

    Shunichi Tayama, Takeshi Kawabe, Yuya Kitamura, Kyoga Hiraide, Jing Li, Ziying Yang, Akihisa Kawajiri, Kosuke Sato, Yuko Okuyama, Mitsuhito Yamada, Masanobu Motrita, Takaaki Akaike, Naoto Ishii

    12th International Conference on the Biology, Chemistry and Therapeutic Applications of Nitric Oxide　2022/10/30

  19. T細胞における新規イオウ代謝の役割

    田山舜一

    第7回FRIS/DIARE Joint Workshop　2022/08/01

  20. CARS2-dependent sulfur metabolism controls intestinal inflammation by suppressing T cell proliferation

    Shunichi Tayama

    KKU-FRIS/DIARE Joint Virtual Workshop for Students　2022/07/06

  21. T細胞におけるイオウ代謝の役割

    田山舜一

    令和4年度前期第2回 全領域合同研究交流会　2022/06/24

  22. Reactive sulfide species generated by cysteinyl-tRNA synthetase plays a regulatory role in T cell-induced colitis in a T cell-intrinsic manner

    Shunichi Tayama

    INTERDISCIPLINARY SEMINAR ON MUCOSAL UMMUNOLOGY AT TOHOKU UNIVERSITY 2022　2022/03/29

  23. T細胞依存的炎症性疾患におけるイオウ代謝経路の役割

    田山舜一

    第14回リトリート大学院生研究発表会　2022/02/28

  24. Reactive sulfide species generated by cysteinyl-tRNA synthetase plays a regulatory role in T cell-induced colitis in a T cell-intrinsic manner

    Shunichi Tayama, Takeshi Kawabe, Yuya Kitamura, Kyoga Hiraide, Jing Li, Ziying Yang, Akihisa Kawajiri, Kosuke Sato, Yuko Okuyama, Masanobu Morita, Takaaki Akaike, Naoto Ishii

    2021/12/09

  25. 自己免疫疾患におけるイオウ代謝の機能解明

    田山舜一

    第6回FRIS/DIARE Joint Workshop　2021/08/02

  26. 自己免疫疾患におけるイオウ代謝の機能解明

    田山舜一

    2021年前期全領域合同交流会　2021/05/14

  27. IQ motif-containing GTPase-activating protein 1 is essential for the optimal maintenance of lung ILC2s

    Shunichi Tayama, Yuko Okuyama, Hai The Phung, Atsuko Asao, Shuhei Kobayashi, Takeshi Kawabe, So Takanori, Naoto Ishii

    Immunology 2020, Cancelled due to COVID-19　2020/05/09

  28. IQGAP1 regulates ILC2 apoptosis in the lung

    Shunichi Tayama

    INTERDISCIPLINARY SEMINOR ON MUCOSAL IMMUNOLOGY AT TOHOKU UNIVERSITY 2020　2020/02/19

  29. イオウ代謝による免疫反応制御

    田山舜一

    第5回FRIS/DIARE Joint Workshop　2020/02/12

  30. T細胞におけるイオウ代謝の機能解明

    田山舜一, 奥山祐子, 河部剛史, 石井直人

    第13回リトリート大学院生研究発表会　2020/01/11

  31. IQGAP1 regulates ILC2 apoptosis in the lung

    Shunichi Tayama, Yuko Okuyama, Hai The Phung, Takanori So, Naoto Ishii

    2019/12/13

  32. 2型自然リンパ球（ILC2）におけるIQGAP1の機能解明

    田山舜一, 奥山祐子, 宗孝紀, 石井直人

    第38回東北免疫研究会　2019/03/08

  33. 2型自然リンパ球（ILC2）におけるIQGAP1の機能解明

    田山舜一

    後期第4回全領域合同研究交流会　2019/01/11

  34. IQGAP1 is essential for ILC2 maintenance in the lung

    Shunichi Tayama, Yuko Okuyama, Takanori, So, Naoto Ishii

    11th Vietnam-Japan Scientific Exchange Meeting　2018/09/15

  35. イネ遺伝子BLADE-ON-PETIOLEタンパクの細胞内局在

    田山舜一, 鳥羽大陽, 楢本悟志, 経塚淳子

    第58回日本植物生理学会年会　2017/03/18

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Research Projects 3

  1. ヒト・マウスに着目した炎症性腸疾患における活性イオウ代謝の包括的理解

    田山 舜一

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 若手研究

    Institution: 東北大学

    2024/04/01 - 2026/03/31

  2. 活性イオウ代謝による腸管炎症制御機構の解明

    田山 舜一

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 研究活動スタート支援

    Institution: 東北大学

    2023/08 - 2025/03

  3. A novel role for sulfur metabolism in T cell

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for JSPS Fellows

    Category: Grant-in-Aid for JSPS Fellows

    Institution: Tohoku University

    2020/04/24 - 2023/03/31