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九十九伸一

徳島大学

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リサーチマップ・
Jグローバル
KAKEN
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2024年9月19日更新

職名: 助教
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学位: 博士(理学)
職歴・経歴: 〜: 徳島大学助手, 大学院ヘルスバイオサイエンス研究部 (-2006.12.)
2013/4: 徳島大学助教, 大学院ヘルスバイオサイエンス研究部 (-2015.3.)
2015/4: 徳島大学助教, 大学院医歯薬学研究部

専門分野・研究分野: ライフサイエンス (Life sciences) [免疫学 (Immunology)]
ライフサイエンス (Life sciences) [分子生物学 (Molecular biology)]

研究者総覧で最新データを確認する

2024年9月19日更新

専門分野・研究分野: ライフサイエンス (Life sciences) [免疫学 (Immunology)]
ライフサイエンス (Life sciences) [分子生物学 (Molecular biology)]
担当経験のある授業科目: ヒューマンサイエンス(病理病態学) (大学院)
免疫学・寄生虫学 (学部)
免疫学・寄生虫学実習 (学部)
寄生虫学・免疫学/寄生虫学実習・免疫学実習 (学部)
細菌学 (学部)
細菌学・細菌学実習 (学部)
細菌学実習 (学部)
指導経験: 研究者総覧に該当データはありませんでした。

研究者総覧で最新データを確認する

2024年9月19日更新

専門分野・研究分野: ライフサイエンス (Life sciences) [免疫学 (Immunology)]
ライフサイエンス (Life sciences) [分子生物学 (Molecular biology)]

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著書

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論文

Thiranut Jaroonwitchawan, Hideki Arimochi, Yuki Sasaki, Chieko Ishifune, Hiroyuki Kondo, Kunihiro Otsuka, Shin-ichi Tsukumo and Koji Yasutomo :
Stimulation of the farnesoid X receptor promotes M2 macrophage polarization.,
Frontiers in Immunology, Vol.14, 2023.

(要約): This skewed polarization towards M2 macrophages by an FXR agonist was accompanied by increased expression of signaling molecules related to the retinoic acid receptor. Inhibition of the retinoic acid receptor suppressed FXR agonist-mediated M2 macrophage polarization, indicating that this polarization was, at least, partly dependent on the retinoic acid receptor pathway. These data demonstrate that FXR has a role in polarization toward M2 macrophages and suggest a possible therapeutic potential of FXR agonists in M2 macrophage-related conditions.
(キーワード): Receptors, Cytoplasmic and Nuclear
(徳島大学機関リポジトリ): ● Metadata: 118291
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fimmu.2023.1065790
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36776885; ● Search Scopus @ Elsevier (PMID): 36776885; ● Search Scopus @ Elsevier (DOI): 10.3389/fimmu.2023.1065790

(徳島大学機関リポジトリ: 118291, DOI: 10.3389/fimmu.2023.1065790, PubMed: 36776885) Yuta Suzuki, Takayuki Miyazaki, Hiroki Muto, Kenji Kubara, Yohei Mukai, Ryuji Watari, Shinya Sato, Keita Kondo, Shin-ichi Tsukumo, Koji Yasutomo, Masashi Ito and Kappei Tsukahara :
Design and lyophilization of lipid nanoparticles for mRNA vaccine and its robust immune response in mice and nonhuman primates.,
Molecular Therapy. Nucleic Acids, Vol.30, 226-240, 2022.

(要約): and identified lead lipid nanoparticles with a branched-tail lipid structure. Buffer optimization allowed the determination of lyophilization conditions, where lipid nanoparticle-encapsulated mRNA encoding SARS-CoV-2 spike protein could induce robust immunogenicity in mice after 1 month of storage at 5°C and 25°C. Intramuscularly injected lipid nanoparticles distributed in conventional dendritic cells in mouse lymph nodes induced balanced T helper (Th) 1/Th2 responses against SARS-CoV-2 spike protein. In nonhuman primates, two doses of 10 or 100 μg of mRNA induced higher spike-specific binding geometric mean titers than those from a panel of SARS-CoV-2-convalescent human sera. Immunized sera broadly inhibited the viral entry receptor angiotensin-converting enzyme 2 (ACE2) from binding to the spike protein in all six strains tested, including variants of concern. These results could provide useful information for designing next-generation mRNA vaccines.
(徳島大学機関リポジトリ): ● Metadata: 117846
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.omtn.2022.09.017
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36187052; ● Search Scopus @ Elsevier (PMID): 36187052; ● Search Scopus @ Elsevier (DOI): 10.1016/j.omtn.2022.09.017

(徳島大学機関リポジトリ: 117846, DOI: 10.1016/j.omtn.2022.09.017, PubMed: 36187052) Shin-ichi Tsukumo, Ganesh Poorani Subramani, Noé Seija, Mizuho Tabata, Yoichi Maekawa, Yuya Mori, Chieko Ishifune, Yasushi Itoh, Mineto Ota, Keishi Fujio, M Noia Javier Di and Koji Yasutomo :
AFF3, a susceptibility factor for autoimmune diseases, is a molecular facilitator of immunoglobulin class switch recombination.,
Science Advances, Vol.8, No.34, 2022.

(要約): in human B cells. These findings demonstrate that AFF3 directly regulates CSR by facilitating the recruitment of AID to the switch regions.
(徳島大学機関リポジトリ): ● Metadata: 117850
(出版サイトへのリンク): ● Publication site (DOI): 10.1126/sciadv.abq0008
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36001653; ● Search Scopus @ Elsevier (PMID): 36001653; ● Search Scopus @ Elsevier (DOI): 10.1126/sciadv.abq0008

(徳島大学機関リポジトリ: 117850, DOI: 10.1126/sciadv.abq0008, PubMed: 36001653) Hiroyuki Kondo, Takahiro Kageyama, Shigeru Tanaka, Kunihiro Otsuka, Shin-ichi Tsukumo, Yoichi Mashimo, Yoshihiro Onouchi, Hiroshi Nakajima and Koji Yasutomo :
Markers of Memory CD8 T Cells Depicting the Effect of the BNT162b2 mRNA COVID-19 Vaccine in Japan.,
Frontiers in Immunology, Vol.13, 2022.

(要約): BNT162b2, a nucleoside-modified mRNA vaccine for SARS-CoV-2 spike glycoprotein (S), provides approximately 95% efficacy for preventing COVID-19. However, it remains unclear how effectively memory CD8+ T cells are generated and which genetic and environmental factors affect the generation and function of memory CD8+ T cells elicited by this vaccine. Here, we investigated the frequency and functions of memory CD8+ T cells 3 weeks after the second vaccination in the Japanese population. Using a peptide-MHC pentamer, we detected an increased number of memory CD8+ T cells together with increased serum anti-S protein antibody in females compared with that in males, but the frequency of pentamer-positive cells was not positively correlated with antibody titers. Memory precursor effector cells (KLRG1-CD127+) among both CD8+ cells and pentamer+ cells and effector cells (CD38-HLA-DR+) among pentamer+ cells were more abundant in females than in males. Upon S protein-mediated stimulation of T cells, the intensity of CD107a and granzyme B expression was increased in females compared with that in males, indicating stronger memory CD8+ T cell responses in females than in males. Our studies showed that the BNT162b2 vaccine elicits increased memory CD8+ T cell proliferation and secondary CTL responses in females compared with those in males in the Japanese population. These findings provide an important basis for the distinct sex difference in cellular immune responses to mRNA vaccination and suggest that memory precursor effector cells can be one of markers to evaluate and boost cellular immunity induced by BNT162b2.
(徳島大学機関リポジトリ): ● Metadata: 117815
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fimmu.2022.836923
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35572546; ● Search Scopus @ Elsevier (PMID): 35572546; ● Search Scopus @ Elsevier (DOI): 10.3389/fimmu.2022.836923

(徳島大学機関リポジトリ: 117815, DOI: 10.3389/fimmu.2022.836923, PubMed: 35572546) Yuki Sasaki, Hideki Arimochi, Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo and Koji Yasutomo :
Blockade of the CXCR3/CXCL10 axis ameliorates inflammation caused by immunoproteasome dysfunction.,
JCI Insight, Vol.7, No.7, 2022.

(要約): Immunoproteasomes regulate the degradation of ubiquitin-coupled proteins and generate peptides that are preferentially presented by MHC class I. Mutations in immunoproteasome subunits lead to immunoproteasome dysfunction, which causes proteasome-associated autoinflammatory syndromes (PRAAS) characterized by nodular erythema and partial lipodystrophy. It remains unclear, however, how immunoproteasome dysfunction leads to inflammatory symptoms. Here, we established mice harboring a mutation in Psmb8 (Psmb8-KI mice) and addressed this question. Psmb8-KI mice showed higher susceptibility to imiquimod-induced skin inflammation (IMS). Blockade of IL-6 or TNF-α partially suppressed IMS in both control and Psmb8-KI mice, but there was still more residual inflammation in the Psmb8-KI mice than in the control mice. DNA microarray analysis showed that treatment of J774 cells with proteasome inhibitors increased the expression of the Cxcl9 and Cxcl10 genes. Deficiency in Cxcr3, the gene encoding the receptor of CXCL9 and CXCL10, in control mice did not change IMS susceptibility, while deficiency in Cxcr3 in Psmb8-KI mice ameliorated IMS. Taken together, these findings demonstrate that this mutation in Psmb8 leads to hyperactivation of the CXCR3 pathway, which is responsible for the increased susceptibility of Psmb8-KI mice to IMS. These data suggest the CXCR3/CXCL10 axis as a new molecular target for treating PRAAS.
(徳島大学機関リポジトリ): ● Metadata: 117226
(出版サイトへのリンク): ● Publication site (DOI): 10.1172/jci.insight.152681
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35393946; ● Search Scopus @ Elsevier (PMID): 35393946; ● Search Scopus @ Elsevier (DOI): 10.1172/jci.insight.152681

(徳島大学機関リポジトリ: 117226, DOI: 10.1172/jci.insight.152681, PubMed: 35393946) Michittra Boonchan, Hideki Arimochi, Kunihiro Otsuka, Tomoko Kobayashi, Hisanori Uehara, Thiranut Jaroonwitchawan, Yuki Sasaki, Shin-ichi Tsukumo and Koji Yasutomo :
Necroptosis protects against exacerbation of acute pancreatitis.,
Cell Death & Disease, Vol.12, No.6, 601, 2021.

(要約): mice exhibit weight loss, edematous pancreatitis, necrotizing pancreatitis, and acinar cell dedifferentiation in response to tissue damage. Genetic deletion of Mlkl resulted in downregulation of the antiapoptotic genes Bclxl and Cflar in association with increases in the numbers of apoptotic cells, as detected by TUNEL assay. These findings suggest that RIPK3 and MLKL-mediated necroptosis exerts protective effects in AP and caution against the use of necroptosis inhibitors for AP treatment.
(徳島大学機関リポジトリ): ● Metadata: 116381
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41419-021-03847-w
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34112763; ● Search Scopus @ Elsevier (PMID): 34112763; ● Search Scopus @ Elsevier (DOI): 10.1038/s41419-021-03847-w

(徳島大学機関リポジトリ: 116381, DOI: 10.1038/s41419-021-03847-w, PubMed: 34112763) Yuki Sasaki, Kunihiro Otsuka, Hideki Arimochi, Shin-ichi Tsukumo and Koji Yasutomo :
Distinct Roles of IL-1 and IL-18 in NLRC4-Induced Autoinflammation.,
Frontiers in Immunology, Vol.11, 591713, 2020.

(要約): The NLRC4 inflammasome assembles in response to detection of bacterial invasion, and NLRC4 activation leads to the production of IL-1 and IL-18 together with pyroptosis-mediated cell death. Missense activating mutations in cause autoinflammatory disorders whose symptoms are distinctly dependent on the site of mutation and other aspects of the genetic background. To determine the involvement of IL-1 and IL-18 in the inflammation induced by mutation, we depleted IL-1 , IL-18, or both cytokines in Nlrc4-transgenic mice in which mutant is expressed under the MHC class II promoter (Nlrc4-H443P-Tg mice). The deletion of the or gene in Nlrc4-H443P-Tg mice reduced the neutrophil numbers in the spleen, and mice with deletion of both genes had an equivalent number of neutrophils compared to wild-type mice. Deletion of ameliorated but did not eliminate bone marrow hyperplasia, while mice deficient in showed no bone marrow hyperplasia. In contrast, tail bone deformity remained in the presence of deficiency, but deficiency completely abolished bone deformity. The decreased bone density in Nlrc4-H443P-Tg mice was counteracted by but not deficiency. Our results demonstrate the distinct effects of IL-1 and IL-18 on NLRC4-induced inflammation among tissues, which suggests that blockers for each cytokine should be utilized depending on the site of inflammation.
(徳島大学機関リポジトリ): ● Metadata: 116191
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fimmu.2020.591713
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33178225; ● Summary page in Scopus @ Elsevier: 2-s2.0-85094604314

(徳島大学機関リポジトリ: 116191, DOI: 10.3389/fimmu.2020.591713, PubMed: 33178225, Elsevier: Scopus) Akio Takezaki, Shin-ichi Tsukumo, Yasuhiro Setoguchi, G Julie Ledford, Hisatsugu Goto, Kazuyoshi Hosomichi, Hisanori Uehara, Yasuhiko Nishioka and Koji Yasutomo :
A homozygous SFTPA1 mutation drives necroptosis of type II alveolar epithelial cells in patients with idiopathic pulmonary fibrosis.,
The Journal of Experimental Medicine, Vol.216, No.12, 2724-2735, 2019.

(要約): promotes necroptosis of AEII cells through JNK-mediated up-regulation of Ripk3, highlighting the necroptosis pathway as a therapeutic target for IPF.
(徳島大学機関リポジトリ): ● Metadata: 114694
(出版サイトへのリンク): ● Publication site (DOI): 10.1084/jem.20182351
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31601679; ● Search Scopus @ Elsevier (PMID): 31601679; ● Search Scopus @ Elsevier (DOI): 10.1084/jem.20182351

(徳島大学機関リポジトリ: 114694, DOI: 10.1084/jem.20182351, PubMed: 31601679) Chieko Ishifune, Shin-ichi Tsukumo, Yoichi Maekawa, Katsuto Hozumi, Hyun Doo Chung, Chihiro Motozono, Sho Yamasaki, Hiroyasu Nakano and Koji Yasutomo :
Regulation of membrane phospholipid asymmetry by Notch-mediated flippase expression controls the number of intraepithelial TCRαβ+CD8αα+ T cells.,
PLoS Biology, Vol.17, No.5, 2019.

(要約): Intestinal intraepithelial lymphocytes (IELs) expressing CD8αα on αβ T cells (TCRαβ+CD8αα+ IELs) have suppressive capabilities in enterocolitis, but the mechanism that maintains homeostasis and cell number is not fully understood. Here, we demonstrated that the number of TCRαβ+CD8αα+ IELs was severely reduced in mice lacking recombination signal binding protein for immunoglobulin kappa J region (Rbpj) or Notch1 and Notch2 in T cells. Rbpj-deficient TCRαβ+CD8αα+ IELs expressed low levels of Atp8a2, which encodes a protein with flippase activity that regulates phospholipid asymmetry of plasma membrane such as flipping phosphatidylserine in the inner leaflet of plasma membrane. Rbpj-deficient TCRαβ+CD8αα+ IELs cannot maintain phosphatidylserine in the inner leaflet of the plasma membrane. Furthermore, depletion of intestinal macrophages restored TCRαβ+CD8αα+ IELs in Rbpj-deficient mice, suggesting that exposure of phosphatidylserine on the plasma membrane in Rbpj-deficient TCRαβ+CD8αα+ IELs acts as an "eat-me" signal. Together, these results revealed that Notch-Atp8a2 is a fundamental regulator for IELs and highlighted that membrane phospholipid asymmetry controlled by Notch-mediated flippase expression is a critical determinant in setting or balancing the number of TCRαβ+CD8αα+ IELs.
(徳島大学機関リポジトリ): ● Metadata: 114327
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pbio.3000262
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31071093; ● Search Scopus @ Elsevier (PMID): 31071093; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pbio.3000262

(徳島大学機関リポジトリ: 114327, DOI: 10.1371/journal.pbio.3000262, PubMed: 31071093) Shin-ichi Tsukumo and Koji Yasutomo :
T Cells and Antitumor Immunity by Notch Signaling.,
Frontiers in Immunology, Vol.9, 2018.

(要約): T cells and discuss issues and implications for its use in antitumor immunity.
(徳島大学機関リポジトリ): ● Metadata: 114462
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fimmu.2018.00101
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29441071; ● Search Scopus @ Elsevier (PMID): 29441071; ● Search Scopus @ Elsevier (DOI): 10.3389/fimmu.2018.00101

(徳島大学機関リポジトリ: 114462, DOI: 10.3389/fimmu.2018.00101, PubMed: 29441071) Masanori Niki, Kohhei Nakajima, Daichi Ishikawa, Jun Nishida, Chieko Ishifune, Shin-ichi Tsukumo, Mitsuo Shimada, Shinji Nagahiro, Yoshinori Mitamura and Koji Yasutomo :
MicroRNA-449a deficiency promotes colon carcinogenesis.,
Scientific Reports, Vol.7, No.1, 10696, 2017.

(要約): MicroRNAs have broad roles in tumorigenesis and cell differentiation through regulation of target genes. Notch signaling also controls cell differentiation and tumorigenesis. However, the mechanisms through which Notch mediates microRNA expression are still unclear. In this study, we aimed to identify microRNAs regulated by Notch signaling. Our analysis found that microRNA-449a (miR-449a) was indirectly regulated by Notch signaling. Although miR-449a-deficient mice did not show any Notch-dependent defects in immune cell development, treatment of miR-449a-deficient mice with azoxymethane (AOM) or dextran sodium sulfate (DSS) increased the numbers and sizes of colon tumors. These effects were associated with an increase in intestinal epithelial cell proliferation following AOM/DSS treatment. In patients with colon cancer, miR-449a expression was inversely correlated with disease-free survival and histological scores and was positively correlated with the expression of MLH1 for which loss-of function mutations have been shown to be involved in colon cancer. Colon tissues of miR-449a-deficient mice showed reduced Mlh1 expression compared with those of wild-type mice. Thus, these data suggested that miR-449a acted as a key regulator of colon tumorigenesis by controlling the proliferation of intestinal epithelial cells. Additionally, activation of miR-449a may represent an effective therapeutic strategy and prognostic marker in colon cancer.
(徳島大学機関リポジトリ): ● Metadata: 112383
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-017-10500-0
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28878284; ● Summary page in Scopus @ Elsevier: 2-s2.0-85029002400

(徳島大学機関リポジトリ: 112383, DOI: 10.1038/s41598-017-10500-0, PubMed: 28878284, Elsevier: Scopus) Sultana Taskia Zaman, Hideki Arimochi, Satoshi Maruyama, Chieko Ishifune, Shin-ichi Tsukumo, Akiko Kitamura and Koji Yasutomo :
Notch Balances Th17 and Induced Regulatory T Cell Functions in Dendritic Cells by Regulating Aldh1a2 Expression.,
The Journal of Immunology, Vol.199, No.6, 1989-1997, 2017.

(要約): Dendritic cells (DCs) are important for adaptive immune responses through the activation of T cells. The molecular interplay between DCs and T cells determines the magnitude of T cell responses or outcomes of functional differentiation of T cells. In this study, we demonstrated that DCs in mice that are Rbpj deficient in CD11c(+) cells (Rbpj(-/-) mice) promoted the differentiation of IL-17A-producing Th17 cells. Rbpj-deficient DCs expressed little Aldh1a2 protein that is required for generating retinoic acid. Those DCs exhibited a reduced ability for differentiating regulatory T cells induced by TGF-. Rbpj protein directly regulated Aldh1a2 transcription by binding to its promoter region. The overexpression of Aldh1a2 in Rbpj-deficient DCs negated their Th17-promoting ability. Transfer of naive CD4(+) T cells into Rag1-deficient Rbpj(-/-) mice enhanced colitis with increased Th17 and reduced induced regulatory T cells (iTreg) compared with control Rag1-deficient mice. The cotransfer of iTreg and naive CD4(+) T cells into Rag1-deficient Rbpj(-/-) mice improved colitis compared with transfer of naive CD4(+) T cell alone. Furthermore, cotransfer of DCs from Rbpj(-/-) mice that overexpressed Aldh1a2 or Notch-stimulated DCs together with naive CD4(+) T cells into Rbpj(-/-)Rag1-deficient mice led to reduced colitis with increased iTreg numbers. Therefore, our studies identify Notch signaling in DCs as a crucial balancer of Th17/iTreg, which depends on the direct regulation of Aldh1a2 transcription in DCs.
(徳島大学機関リポジトリ): ● Metadata: 110921
(出版サイトへのリンク): ● Publication site (DOI): 10.4049/jimmunol.1700645
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28779023; ● Search Scopus @ Elsevier (PMID): 28779023; ● Search Scopus @ Elsevier (DOI): 10.4049/jimmunol.1700645

(徳島大学機関リポジトリ: 110921, DOI: 10.4049/jimmunol.1700645, PubMed: 28779023) Takahiro Furukawa, Chieko Ishifune, Shin-ichi Tsukumo, Katsuto Hozumi, Yoichi Maekawa, Naoko Matsui, Ryuji Kaji and Koji Yasutomo :
Transmission of survival signals through Delta-like 1 on activated CD4(+) T cells.,
Scientific Reports, Vol.6, 33692, 2016.

(要約): Notch expressed on CD4(+) T cells transduces signals that mediate their effector functions and survival. Although Notch signaling is known to be cis-inhibited by Notch ligands expressed on the same cells, the role of Notch ligands on T cells remains unclear. In this report we demonstrate that the CD4(+) T cell Notch ligand Dll1 transduces signals required for their survival. Co-transfer of CD4(+) T cells from Dll1(-/-) and control mice into recipient mice followed by immunization revealed a rapid decline of CD4(+) T cells from Dll1(-/-) mice compared with control cells. Dll1(-/-) mice exhibited lower clinical scores of experimental autoimmune encephalitis than control mice. The expression of Notch target genes in CD4(+) T cells from Dll1(-/-) mice was not affected, suggesting that Dll1 deficiency in T cells does not affect cis Notch signaling. Overexpression of the intracellular domain of Dll1 in Dll1-deficient CD4(+) T cells partially rescued impaired survival. Our data demonstrate that Dll1 is an independent regulator of Notch-signaling important for the survival of activated CD4(+) T cells, and provide new insight into the physiological roles of Notch ligands as well as a regulatory mechanism important for maintaining adaptive immune responses.
(徳島大学機関リポジトリ): ● Metadata: 112325
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/srep33692
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27659682; ● Summary page in Scopus @ Elsevier: 2-s2.0-84988568998

(徳島大学機関リポジトリ: 112325, DOI: 10.1038/srep33692, PubMed: 27659682, Elsevier: Scopus) Yoichi Maekawa, Chieko Ishifune, Shin-ichi Tsukumo, Katsuto Hozumi, Hideo Yagita and Koji Yasutomo :
Notch controls the survival of memory CD4+ T cells by regulating glucose uptake.,
Nature Medicine, Vol.21, No.1, 55-61, 2015.

(要約): CD4+ T cells differentiate into memory T cells that protect the host from subsequent infection. In contrast, autoreactive memory CD4+ T cells harm the body by persisting in the tissues. The underlying pathways controlling the maintenance of memory CD4+ T cells remain undefined. We show here that memory CD4+ T cell survival is impaired in the absence of the Notch signaling protein known as recombination signal binding protein for immunoglobulin J region (Rbpj). Treatment of mice with a Notch inhibitor reduced memory CD4+ T cell numbers and prevented the recurrent induction of experimental autoimmune encephalomyelitis. Rbpj-deficient CD4+ memory T cells exhibit reduced glucose uptake due to impaired AKT phosphorylation, resulting in low Glut1 expression. Treating mice with pyruvic acid, which bypasses glucose uptake and supplies the metabolite downstream of glucose uptake, inhibited the decrease of autoimmune memory CD4+ T cells in the absence of Notch signaling, suggesting memory CD4+ T cell survival relies on glucose metabolism. Together, these data define a central role for Notch signaling in maintaining memory CD4+ T cells through the regulation of glucose uptake.
(キーワード): Animals / CD4-Positive T-Lymphocytes / Glucose / Glucose Transporter Type 1 / Humans / Immunoglobulin J Recombination Signal Sequence-Binding Protein / Mice / Oncogene Protein v-akt / Receptors, Antigen, T-Cell / Receptors, Notch / Signal Transduction
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/nm.3758
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25501905; ● Summary page in Scopus @ Elsevier: 2-s2.0-84925284022

(DOI: 10.1038/nm.3758, PubMed: 25501905, Elsevier: Scopus) Hiroyuki Kose, Tohru Sakai, Shin-ichi Tsukumo, Kaichun Wei, Takahisa Yamada, Koji Yasutomo and Kozo Matsumoto :
Maturational arrest of thymocyte development is caused by a deletion in the receptor-like protein tyrosine phosphatase κ gene in LEC rats,
Genomics, Vol.89, No.6, 673-677, 2007.

(要約): The Long-Evans Cinnamon (LEC) rat has a spontaneous mutation, T helper immunodeficiency (thid), which causes a markedly reduced CD4(+) thymocyte population. Here we positionally clone the locus and identify a deletion in the gene encoding a receptor-like protein tyrosine phosphatase kappa (Ptprk) that led to complete loss of the transcript. The rat Ptprk gene exhibits 98% identity with the human and mouse counterparts and is expressed most abundantly in the CD4(-)CD8(-) double-negative stage. The downregulation of Ptprk in mouse immature thymocytes by RNA interference mimicked the thid phenotype. These results indicate that thid maps to the Ptprk locus and that functional Ptprk is crucial for lineage commitment or progression of CD4(+) T cells. We also found that Ptprk appears to function in parallel with or downstream of Th-POK/cKrox (also known as ZBTB7B), a master regulator of T cell lineage decision.
(キーワード): T cell differentiation / Protein phosphatase / LEC rat / Thymus / Th-POK/cKrox
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ygeno.2007.03.001
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17434290; ● Search Scopus @ Elsevier (PMID): 17434290; ● Search Scopus @ Elsevier (DOI): 10.1016/j.ygeno.2007.03.001

(DOI: 10.1016/j.ygeno.2007.03.001, PubMed: 17434290) Yuki Hayashi, Naozumi Ishimaru, Rieko Arakaki, Shin-ichi Tsukumo, Hitomi Fukui, Kenji Kishihara, Hiroshi Shiota, Koji Yasutomo and Yoshio Hayashi :
Effective Treatment of a Mouse Model of Sjogren's Syndrome With Eyedrop Administrasiton of Anti-CD4 Monoclonal Antibody,
Arthritis and Rheumatism, Vol.50, No.9, 2903-2910, 2004.

(要約): To determine whether eyedrop administration of an anti-CD4 monoclonal antibody (mAb) is effective in the treatment of Sjögren's syndrome (SS) using a mouse model of the disease. The anti-CD4 mAb was administered daily into the eyes of mice with SS from ages 4 to 8 weeks or ages 10 to 12 weeks. During treatment, tear volume was monitored and after final treatment, histologic features of the lacrimal and salivary glands, the phenotypes and function of T cells, and serum titers of anti-alpha-fodrin antibody were examined. Eyedrop administration of anti-CD4 mAb before the onset of SS prevented the autoimmune pathology seen in the lacrimal glands but not that in the salivary glands. Furthermore, eyedrop administration of anti-CD4 mAb after the development of SS inhibited mononuclear cell infiltration and the destruction of parenchyma only in the lacrimal glands. Eyedrop administration of anti-CD4 mAb suppressed the local activation of CD4+ T cells rather than deleting CD4+ T cells, which reduced the expansion of pathologic CD4+ T cells against alpha-fodrin. These results demonstrate the remarkable efficacy of anti-CD4 mAb eyedrops in the treatment of SS eye symptoms, which illustrates a new antibody-based therapeutic strategy for patients with eye problems caused by SS as well as other diseases.
(キーワード): Administration, Topical / Animals / Antibodies, Monoclonal / Antigens, CD4 / CD4-Positive T-Lymphocytes / Disease Progression / Dry Eye Syndromes / Female / Lacrimal Apparatus / Lymphocyte Activation / Mice / Models, Animal / Ophthalmic Solutions / 唾液腺 (salivary glands) / シェーグレン症候群 (Sjögren's syndrome) / Treatment Outcome
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/art.20472
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15457459; ● Search Scopus @ Elsevier (PMID): 15457459; ● Search Scopus @ Elsevier (DOI): 10.1002/art.20472

(DOI: 10.1002/art.20472, PubMed: 15457459) Yuki Hayashi, Shin-ichi Tsukumo, Hiroshi Shiota, Kenji Kishihara and Koji Yasutomo :
Antigen-Specific T Cell Repertoire Modification of CD4⁺CD25⁺ Regulatory T Cells,
The Journal of Immunology, Vol.172, No.9, 5240-5248, 2004.

(要約): T cell immune responses are regulated by the interplay between effector and suppressor T cells. Immunization with Ag leads to the selective expansion and survival of effector CD4(+) T cells with high affinity TCR against the Ag and MHC. However, it is not known if CD4(+)CD25(+) regulatory T cells (T(reg)) recognize the same Ag as effector T cells or whether Ag-specific TCR repertoire modification occurs in T(reg). In this study, we demonstrate that after a primary Ag challenge, T(reg) proliferate and TCR repertoire modification is observed although both of these responses were lower than those in conventional T cells. The repertoire modification of Ag-specific T(reg) after primary Ag challenge augmented the total suppressive function of T(reg) against TCR repertoire modification but not against the proliferation of memory CD4(+) T cells. These results reveal that T cell repertoire modification against a non-self Ag occurs in T(reg), which would be crucial for limiting excess primary and memory CD4(+) T cell responses. In addition, these studies provide evidence that manipulation of Ag-specific T(reg) is an ideal strategy for the clinical use of T(reg).
(キーワード): Animals / Antigen Presentation / Antigens / CD4-Positive T-Lymphocytes / 細胞分化 (cell differentiation) / 細胞分裂 (cell division) / Cells, Cultured / Columbidae / Complementarity Determining Regions / Cytochromes c / Epitopes, T-Lymphocyte / Immunization, Secondary / Immunologic Memory / Lymphocyte Count / Mice / Mice, Inbred A / Mice, Inbred C57BL / Receptors, Antigen, T-Cell, alpha-beta / T-Lymphocytes, Regulatory
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15100262; ● Search Scopus @ Elsevier (PMID): 15100262

(PubMed: 15100262) Yoichi Maekawa, Shin-ichi Tsukumo, Okada Hiroko, Kenji Kishihara and Koji Yasutomo :
Breakdown of peripheral T-cell tolerance by chronic IL-15 elevation,
Transplantation, Vol.76, No.2, 415-420, 2003.

(要約): Thymic deletion purges the repertoire of most developing T cells with the potential for overt self-reactivity, but some self-specific cells do emerge into the peripheral pool. Under most conditions, these potentially autoaggressive cells remain in a quiescent state. However, in some circumstances, they become activated and acquire effector function, leading to immune disease. It is thus important to clarify the mechanism(s) responsible for determining the balance between such inappropriate T-cell activation and the normal state of peripheral tolerance. In this article, we show that chronic elevation of interleukin-15 levels interferes with the tolerant state of CD8+ T cells through a process that involves activation of nonlymphoid antigen-presenting cells by CD4+asialo-GM1+ (ASGM1) or both CD4+ASGM1- and CD4-ASGM1+ cells. These findings suggest a potential role for dysregulated interleukin-15 production in promoting tolerance breakdown. This new information may be of potential use in improving tumor vaccines to self-antigens and in ameliorating autoimmune or graft-versus-host disease.
(キーワード): Animals / CD4-Positive T-Lymphocytes / CD8-Positive T-Lymphocytes / Fetal Tissue Transplantation / Graft vs Host Disease / Hematopoietic Stem Cell Transplantation / Immune Tolerance / Interleukin-15 / Liver / Lymphocyte Activation / Mice / Mice, Inbred AKR / Mice, SCID / Spleen / Thymus Gland / Transplantation Chimera
(出版サイトへのリンク): ● Publication site (DOI): 10.1097/01.TP.0000078900.71840.2B
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12883202; ● Search Scopus @ Elsevier (PMID): 12883202; ● Search Scopus @ Elsevier (DOI): 10.1097/01.TP.0000078900.71840.2B

(DOI: 10.1097/01.TP.0000078900.71840.2B, PubMed: 12883202)

MISC

研究者総覧に該当データはありませんでした。

総説・解説

九十九伸一, 安友康二 :
メモリーT細胞と代謝 (特集免疫と代謝),
臨床免疫·アレルギー科, Vol.73, No.5, 456-460, 2020年5月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1523669554862108032

(CiNii: 1523669554862108032) 九十九伸一, 安友康二 :
Notchシグナルによる細胞内代謝制御 (特集免疫系を介したシステム連関 : 恒常性の維持と破綻) -- (免疫細胞における代謝調節),
生体の科学, Vol.70, No.2, 109-113, 2019年3月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1520291856004810240

(CiNii: 1520291856004810240)

講演・発表

Chieko Ishifune, Shin-ichi Tsukumo and Koji Yasutomo :
Notch signal controls the number of TCR+CD8+ intraepithelial lymphocytes via phospholipid asymmetry by maintaining flippase ATP8a2,
Australia-Japan Meeting on Cell Death, Tokyo, May 2018. Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo, Aya Ushio, Naozumi Ishimaru and Koji Yasutomo :
CD153+ CD4+ T cells and CD30+ cells exacerbate the autoimmune pathology in salivary glands of Sjögren's syndrome,
第52回日本免疫学会学術集会, Jan. 2024. Shin-ichi Tsukumo and Koji Yasutomo :
The functions of transcription elongation factor Cdk9 in T cells,
第52回日本免疫学会学術集会, Jan. 2024. 大塚邦紘, 近藤博之, 九十九伸一, 牛尾綾, 永尾瑠佳, 青田桂子, 石丸直澄, 安友康二 :
シングルセル解析を基盤としたシェーグレン症候群の病態解明,
第31回日本シェーグレン症候群学会学術集会, 2023年9月. 鈴木裕太, 宮崎崇之, 武藤洋樹, 久原健嗣, 向洋平, 渡隆爾, 佐藤晋也, 近藤啓太, 九十九伸一, 安友康二, 伊藤昌史, 塚原克平 :
mRNAワクチンの脂質ナノ粒子設計と凍結乾燥,
第 39 回日本 DDS 学会学術集会, 2023年7月. 鈴木裕太, 宮崎崇之, 武藤洋樹, 久原健嗣, 向洋平, 渡隆爾, 佐藤晋也, 近藤啓太, 九十九伸一, 安友康二, 伊藤昌史, 塚原克平 :
mRNAワクチンの脂質ナノ粒子設計と凍結乾燥,
第8回日本核酸医薬学会, 2023年7月. 大塚邦紘, 近藤博之, 九十九伸一, 新垣理恵子, 永尾瑠佳, 佐藤真美, 牛尾綾, 石丸直澄, 安友康二 :
CD153-CD30相互反応を介したシェーグレン症候群の病態形成機構の解明,
第112回日本病理学会総会, 2023年4月. Kunihiro Otsuka, Shin-ichi Tsukumo, Rieko Arakaki, Mami Sato, 八木田秀雄, Naozumi Ishimaru and Koji Yasutomo :
CD153+ CD4+ T cells exacerbate the autoimmune pathology via the interaction with CD30+ cells in salivary glands in Sjögren's syndrome.,
第51回日本免疫学会学術集会, Dec. 2022. 近藤博之, 九十九伸一, 大塚邦紘, 安友康二 :
Markers of memory CD8 T cells depicting the effect of the BNT162b2 mRNA COVID-19 vaccine in Japan,
第45回日本分子生物学会年会, 2022年11月. 大塚邦紘, 近藤博之, 九十九伸一, 新垣理恵子, 佐藤真美, 常松貴明, 石丸直澄, 安友康二 :
シングルセルRNA-seqとマルチプレックスSpatial解析を基盤としたシェーグレン症候群の標的臓器微小環境変化の解明,
第33回日本臨床口腔病理学会, 2022年9月. 大塚邦紘, 九十九伸一, 近藤博之, 佐藤真美, 俵宏彰, 常松貴明, 石丸直澄, 安友康二 :
シングルセルRNA-seqで紐解くシェーグレン症候群モデルに特徴的に出現するT細胞集団の解析,
第64回歯科基礎医学会学術大会, 2022年9月. 近藤博之, 大塚邦紘, 九十九伸一, 安友康二 :
日本における新型SARS-CoV-2 mRNAワクチンBNT162b2の効果を示すメモリーCD8T細胞マーカー,
第20回四国免疫フォーラム, 2022年6月. 大塚邦紘, 九十九伸一, 近藤博之, 新垣理恵子, 石丸直澄, 安友康二 :
シングルセルRNA-seqで紐解くシェーグレン症候群モデルに特徴的に出現するT細胞集団の解析,
第111回日本病理学会総会, 2022年4月. 細山田翔太, 九十九伸一, 加治佐平, 安友康二, 安井武史 :
プラズモニクスバイオセンサを用いたエクソソーム中のマイクロRNA断片の超高感度検出,
第69回応用物理学会春季学術講演会, 24p-E104-2, 2022年3月. Kunihiro Otsuka, Shin-ichi Tsukumo, Rieko Arakaki, Mami Sato, Hideo Yagita, Naozumi Ishimaru and Koji Yasutomo :
Single-cell RNA sequencing reveals accumulation of CD4 and CD8 T cells with unique phenotypes in salivary glands of Sjögren's syndrome model mice,
第50回日本免疫学会学術集会, Dec. 2021. Yuki Sasaki, Hideki Arimochi, Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo and Koji Yasutomo :
Blockade of the CXCR3-CXCL10 axis ameliorates inflammatory responses caused by immunoproteasome dysfunctions,
第50回日本免疫学会学術集会, Dec. 2021. Shin-ichi Tsukumo, Yoichi Maekawa, Fujio Keishi and Koji Yasutomo :
AFF3 regulates class switch recombination by enhacing mutagenesis of switch region,
第50回日本免疫学会学術集会, Dec. 2021. Boonchan Michittra, Hideki Arimochi, Kunihiro Otsuka, Tomoko Kobayashi, Hisanori Uehara, Jaroonwitchawan Thiranut, Yuki Sasaki, Shin-ichi Tsukumo and Koji Yasutomo :
Deficiency in Ripk3 or Mlkl exacerbates acute pancreatitis with increased apoptosis of acinar cell,
第19回四国免疫フォーラム, Jun. 2021. 加治佐平, 矢野隆章, 大塚邦紘, 九十九伸一, 坂根亜由子, 駒貴明, 野間口雅子, 安友康二, 佐々木卓也, 安井武史 :
SARS-CoV-2由来RNAの高感度検出に向けたプラズモニックバイオセンサ,
第68回応用物理学会春季学術講演会予稿集, 16p-Z22-13, 2021年3月. Shin-ichi Tsukumo, Yoichi Maekawa and Koji Yasutomo :
Aff3 is required for the class switching of IgG2c, IgG1 and IgG3 in a B cell-intrinsic manner,
第48回日本免疫学会学術集会, Dec. 2019. Shin-ichi Tsukumo and Koji Yasutomo :
Transcriptional elongation factor Aff3 regulates class switching of antibody in B cells,
第47回日本免疫学会学術集会, Dec. 2018. 九十九伸一, 安友康二 :
自己免疫疾患におけるAFFファミリーの役割,
第33回自己免疫研究会, 2018年7月. Chieko Ishifune, Shin-ichi Tsukumo and Koji Yasutomo :
Notch signal controls the number of TCRab+CD8aa+ intraepithelial lymphocytes via phospholipid asymmetry by maintaining flippase ATP8a2,
第46回日本免疫学会学術集会, Dec. 2017. Shin-ichi Tsukumo and Koji Yasutomo :
DNA結合因子 CTCFのCD4 T細胞における役割,
第31回自己免疫研究会, Jul. 2016. Shin-ichi Tsukumo and Koji Yasutomo :
Function of Notch-Rbpj pathway in naive CD8 T cells,
第44回日本免疫学会学術集会, Nov. 2015. Shin-ichi Tsukumo and Koji Yasutomo :
Notch-Rbpj target genes for maintaining naive and memory T cells,
第43回日本免疫学会学術集会, Dec. 2014.

研究会・報告書: 研究者総覧に該当データはありませんでした。

特許: 研究者総覧に該当データはありませんでした。
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補助金・競争的資金: CDK9タンパク質のAFF依存的および非依存的機能とその制御機構 (研究課題/領域番号: 23K06379 )
関節リウマチと転写伸長遺伝子Aff3の関連についての解析 (研究課題/領域番号: 18K08388 )
異なるリガンド環境におけるTリンパ球応答の分子基盤 (研究課題/領域番号: 18060031 )
糖鎖修飾によるNotchシグナルの修飾とそのTリンパ球における役割 (研究課題/領域番号: 17790322 )
NotchシグナルによるTリンパ球活性化制御機構の解明 (研究課題/領域番号: 17047027 )
Notch分子の糖鎖修飾によるT細胞分化への影響 (研究課題/領域番号: 17046013 )
Notchリガンドを用いた新規癌免疫療法の開発 (研究課題/領域番号: 17016052 )
Notchレセプター糖鎖転移酵素フリンジのTリンパ球特異的ジーン・ターゲティング (研究課題/領域番号: 16590407 )
Notch分子によるヘルパーTリンパ球分化・活性化制御機構の解明 (研究課題/領域番号: 16017271 )
Jagged1を制御することによる癌免疫の増強に関する研究 (研究課題/領域番号: 15025253 )
Tリンパ球の生死を規定する分子機構の解明 (研究課題/領域番号: 14033233 )
制御性T細胞を用いた抗腫瘍免疫の増強効果に関する研究 (研究課題/領域番号: 14030061 )
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専門分野・研究分野: ライフサイエンス (Life sciences) [免疫学 (Immunology)]
ライフサイエンス (Life sciences) [分子生物学 (Molecular biology)]
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受賞: 2024年2月, 康楽賞 (財団法人三木康楽会)
活動: 遺伝子組換え実験安全管理委員会委員 (2017年2月〜2023年)

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Jグローバル最終確認日: 2024/9/14 01:23
氏名（漢字）: 九十九伸一
氏名（フリガナ）: ツクモシンイチ
氏名（英字）: Tsukumo Shin-ichi
所属機関: 徳島大学助教
徳島大学助教

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researchmap最終確認日: 2024/9/15 01:42
氏名（漢字）: 九十九伸一
氏名（フリガナ）: ツクモシンイチ
氏名（英字）: Tsukumo Shin-ichi
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所属: 徳島大学
部署: 医歯薬学研究部生体防御医学分野
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研究者番号: 10346596

所属（現在）: 2024/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 助教

所属（過去の研究課題 情報に基づく）*注記: 2023/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 助教
2018/4/1 – 2020/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 助教
2005/4/1 – 2006/4/1 : 徳島大学, 大学院ヘルスバイオサイエンス研究部, 助手
2004/4/1 – 2006/4/1 : 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助手
2004/4/1 : 徳島大学, ヘルスバイオサイエンス研究部, 助手
2002/4/1 – 2003/4/1 : 徳島大学, 医学部, 助手

審査区分/研究分野

研究代表者

生物系 / 医歯薬学 / 基礎医学 / 免疫学
小区分54020:膠原病およびアレルギー内科学関連
小区分48040:医化学関連

研究代表者以外

生物系 / 医歯薬学 / 基礎医学 / 免疫学
生物系

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研究代表者

T細胞分化 / Notch / 糖鎖修飾 / Fringe / 細胞系譜 / 分子生物学 / 細胞分化 / Tリンパ球 / 抗体 / クラススイッチ / 自己免疫疾患 / 転写伸長 / B細胞 / 関節リウマチ / 転写伸長因子 / 免疫疾患 / リンパ球 / がん

研究代表者以外

癌 / 免疫学 / 細胞・組織 / 病理学 / 内科 / アポトーシス / T細胞 / 不死化 / 免疫寛容 / シグナル伝達 / 発生・分化 / Notch / 免疫療法 / 樹状細胞 / Tリンパ球 / Jagged / CD8 / 膠原病 / 腫瘍免疫 / 細胞分化 / 細胞系譜決定 / Th1 / Th2 / CTL / 細胞内寄生性病原体 / 細胞療法 / CD4 / 糖鎖 / fringe / 免疫応答 / リガンド結合 / フリンジ / ジーンターゲティング / 遺伝子改変 / 細胞系譜 / ジーン・ターゲティング / 糖鎖転移酵素 / lunatic fringe / glycosylation / T lymphocyte development / gene targeting / cell fate decision / thymic organ culture / cell sutonomous regulation

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九十九 伸一

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九十九伸一