田中 努 (タナカ ツトム)

医学研究院 病理系部門 微生物学免疫学分野助教
総合イノベ-ション創発機構ワクチン研究開発拠点助教
Last Updated :2025/12/04

■研究者基本情報

学位

  • 博士 (獣医学), 山口大学, 2015年09月

Researchmap個人ページ

研究キーワード

  • 自己免疫
  • 癌免疫

研究分野

  • ライフサイエンス, 分子生物学
  • ライフサイエンス, 免疫学
  • ライフサイエンス, 腫瘍生物学

担当教育組織

■経歴

経歴

  • 2022年10月 - 現在
    北海道大学, 医学研究院 病理系部門 微生物学免疫学分野, 助教
  • 2021年10月 - 2022年09月
    米国立衛生研究所, 研究員
  • 2016年10月 - 2021年09月
    米国立衛生研究所, 博士研究員
  • 2018年03月 - 2020年02月
    米国衛生研究所, JSPS-NIH Research Fellow
  • 2015年10月 - 2016年09月
    北海道大学, 遺伝子病制御研究所, 博士研究員

学歴

  • 2012年04月 - 2015年09月, 山口大学, 大学院連合獣医学研究科
  • 2006年04月 - 2012年03月, 鳥取大学, 農学部, 獣医学科 (現: 共同獣医学科)

■研究活動情報

受賞

  • 2020年, NIH Fellows Award for Research Excellence (FARE)               
  • 2014年11月, 日本臨床ストレス応答学会, 若手研究奨励賞               
    田中 努

論文

  • Investigation of Lysosome‐Associated Membrane Protein 3 Highlighting the Role of Lysosome in Pathophysiology and Treatment of Sjögren Disease
    Hiroyuki Nakamura, Tsutomu Tanaka, Masayuki Noguchi, Tatsuya Atsumi, Blake M. Warner, John A. Chiorini
    Arthritis & Rheumatology, 2025年11月30日
    研究論文(学術雑誌)
  • Amplified Type I Interferon Response in Sjögren's Disease via Ectopic Toll‐Like Receptor 7 Expression in Salivary Gland Epithelial Cells Induced by Lysosome‐Associated Membrane Protein 3
    Hiroyuki Nakamura, Tsutomu Tanaka, Changyu Zheng, Sandra A. Afione, Tatsuya Atsumi, Masayuki Noguchi, Fabiola Reis Oliveira, Ana Carolina F. Motta, Fernando Chahud, Eduardo M. Rocha, Blake M. Warner, John A. Chiorini
    Arthritis & Rheumatology, 2024年07月
    研究論文(学術雑誌)
  • The balance between nuclear import and export of NLRC5 regulates MHC class I transactivation
    Baohui Zhu, Ryota Ouda, Ning An, Tsutomu Tanaka, Koichi S. Kobayashi
    Journal of Biological Chemistry, 2024年05月
    研究論文(学術雑誌)
  • Lysosome‐Associated Membrane Protein 3 Induces Lysosome‐Dependent Cell Death by Impairing Autophagic Caspase 8 Degradation in the Salivary Glands of Individuals With Sjögren's Disease
    Hiroyuki Nakamura, Tsutomu Tanaka, Changyu Zheng, Sandra A. Afione, Blake M. Warner, Masayuki Noguchi, Tatsuya Atsumi, John A. Chiorini
    Arthritis & Rheumatology, 2023年09月, [筆頭著者]
    研究論文(学術雑誌)
  • Salivary gland LAMP3 mRNA expression is a possible predictive marker in the response to hydroxychloroquine in Sjögren’s disease
    Hiroyuki Nakamura, Tsutomu Tanaka, Youngmi Ji, Changyu Zheng, Sandra A. Afione, Blake M. Warner, Fabiola Reis Oliveira, Ana Carolina F. Motta, Eduardo M. Rocha, Masayuki Noguchi, Tatsuya Atsumi, John A. Chiorini
    PLOS ONE, 18, 2, Public Library of Science ({PLoS}), 2023年02月23日, [筆頭著者]
    英語, 研究論文(学術雑誌), Hydroxychloroquine (HCQ) is a lysosomotropic agent that is commonly used for treating Sjögren’s disease (SjD). However, its efficacy is controversial because of the divergent response to the drug among patients. In a subgroup of SjD patients, lysosome-associated membrane protein 3 (LAMP3) is elevated in expression in the salivary glands and promotes lysosomal dysregulation and lysosome-dependent apoptotic cell death. In this study, chloroquine (CQ) and its derivative HCQ were tested for their ability to prevent LAMP3-induced apoptosis, in vitro and on a mouse model of SjD. In addition, efficacy of HCQ treatment was retrospectively compared between high LAMP3 mRNA expression in minor salivary glands and those with LAMP3 mRNA levels comparable with healthy controls. Study results show that CQ treatment stabilized the lysosomal membrane in LAMP3-overexpressing cells via deactivation of cathepsin B, resulting in decreased apoptotic cell death. In mice with established SjD-like phenotype, HCQ treatment also significantly decreased apoptotic cell death and ameliorated salivary gland hypofunction. Retrospective analysis of SjD patients found that HCQ tended to be more effective in improving disease activity index, symptom severity and hypergammaglobulinemia in patients with high LAMP3 expression compared those with normal LAMP3 expression. Taken together, these findings suggested that by determining salivary gland LAMP3 mRNA level, a patient’s response to HCQ treatment could be predicted. This finding may provide a novel strategy for guiding the development of more personalized medicine for SjD.
  • LAMP3 transfer via extracellular particles induces apoptosis in Sjögren’s disease
    Tsutomu Tanaka, Hiroyuki Nakamura, Duy T. Tran, Blake M. Warner, Yan Wang, Tatsuya Atsumi, Masayuki Noguchi, John A. Chiorini
    Scientific Reports, 13, 1, Springer Science and Business Media {LLC}, 2023年02月14日, [筆頭著者]
    英語, 研究論文(学術雑誌), AbstractSjögren’s disease (SjD) is an autoimmune disease that affects exocrine tissues and is characterized by increased apoptosis in salivary and lacrimal glands. Although the pathogenic mechanism triggering SjD is not well understood, overexpression of lysosome-associated membrane protein 3 (LAMP3) is associated with the disease in a subset of SjD patients and the development of SjD-like phenotype in mice. In this study, histological analysis of minor salivary glands of SjD patients suggested that LAMP3-containing material is being ejected from cells. Follow-on in vitro experiments with cells exposed to extracellular particles (EPs) derived from LAMP3-overexpressing cells showed increased apoptosis. Proteomics identified LAMP3 as a major component of EPs derived from LAMP3-overexpressing cells. Live-cell imaging visualized release and uptake of LAMP3-containing EPs from LAMP3-overexpressing cells to naïve cells. Furthermore, experiments with recombinant LAMP3 protein alone or complexed with Xfect protein transfection reagent demonstrated that internalization of LAMP3 was required for apoptosis in a caspase-dependent pathway. Taken together, we identified a new role for extracellular LAMP3 in cell-to-cell communication via EPs, which provides further support for targeting LAMP3 as a therapeutic approach in SjD.
  • Association of G protein‐coupled receptor 78 with salivary dysfunction in male Sjögren's patients
    Tsutomu Tanaka, Maria Cambraia Guimaro Diniz, Hiroyuki Nakamura, Paola Perez, Youngmi Ji, Drew G. Michael, Sandra A. Afione, Changyu Zheng, Corinne Goldsmith, William D. Swaim, Anne Marie Lynge Pedersen, John A. Chiorini
    Oral Diseases, Wiley, 2023年01月18日, [筆頭著者]
    英語, 研究論文(学術雑誌)
  • Correction of LAMP3-associated salivary gland hypofunction by aquaporin gene therapy
    Hiroyuki Nakamura, Tsutomu Tanaka, Changyu Zheng, Sandra A. Afione, Blake M. Warner, Masayuki Noguchi, Tatsuya Atsumi, John A. Chiorini
    Scientific Reports, 12, 1, 18570, Springer Science and Business Media {LLC}, 2022年11月03日, [筆頭著者]
    英語, 研究論文(学術雑誌), AbstractSjögren’s disease (SjD) is a chronic autoimmune sialadenitis resulting in salivary gland hypofunction with dry mouth symptom. Previous studies showed that lysosome-associated membrane protein 3 (LAMP3) overexpression is involved in the development of salivary gland hypofunction associated with SjD. However, the molecular mechanisms are still unclear, and no effective treatment exists to reverse gland function in SjD. Analysis on salivary gland samples from SjD patients showed that salivary gland hypofunction was associated with decreased expression of sodium–potassium-chloride cotransporter-1 (NKCC1) and aquaporin 5 (AQP5), which are membrane proteins involved in salivation. Further studies revealed that LAMP3 overexpression decreased their expression levels by promoting endolysosomal degradation. Additionally, we found that LAMP3 overexpression enhanced gene transfer by increasing internalization of adeno-associated virus serotype 2 (AAV2) via the promoted endolysosomal pathway. Retrograde cannulation of AAV2 vectors encoding AQP1 gene (AAV2-AQP1) into salivary glands induced glandular AQP1 expression sufficient to restore salivary flow in LAMP3-overexpressing mice. LAMP3 could play a critical role in the development of salivary gland hypofunction in SjD by promoting endolysosomal degradation of NKCC1 and AQP5. But it also could enhance AAV2-mediated gene transfer to restore fluid movement through induction of AQP1 expression. These findings suggested that AAV2-AQP1 gene therapy is useful in reversing salivary gland function in SjD patients.
  • Indocyanine green conjugated phototheranostic nanoparticle for photodiagnosis and photodynamic therapy
    Kenta Shinoda, Akiko Suganami, Yasumitsu Moriya, Masamichi Yamashita, Tsutomu Tanaka, Akane S. Suzuki, Hiroshi Suito, Yasunori Akutsu, Kengo Saito, Yoko Shinozaki, Kazuoki Isojima, Naohito Nakamura, Yasushi Miyauchi, Hiroshi Shirasawa, Hisahiro Matsubara, Yoshiharu Okamoto, Toshinori Nakayama, Yutaka Tamura
    Photodiagnosis and Photodynamic Therapy, 39, 103041, 103041, Elsevier {BV}, 2022年09月
    英語, 研究論文(学術雑誌)
  • Enteric viruses replicate in salivary glands and infect through saliva
    S. Ghosh, M. Kumar, M. Santiana, A. Mishra, M. Zhang, H. Labayo, A. M. Chibly, H. Nakamura, T. Tanaka, W. Henderson, E. Lewis, O. Voss, Y. Su, Y. Belkaid, J. A. Chiorini, M. P. Hoffman, N. Altan-Bonnet
    Nature, 2022年07月14日
    研究論文(学術雑誌)
  • Lysosomal exocytosis of HSP70 stimulates monocytic BMP6 expression in Sjögren’s syndrome
    Ying-Qian Mo, Hiroyuki Nakamura, Tsutomu Tanaka, Toshio Odani, Paola Perez, Youngmi Ji, Benjamin N. French, Thomas J.F. Pranzatelli, Drew G. Michael, Hongen Yin, Susan S. Chow, Maryam Khalaj, Sandra A. Afione, Changyu Zheng, Fabiola Reis Oliveira, Ana Carolina F. Motta, Alfredo Ribeiro-Silva, Eduardo M. Rocha, Cuong Q. Nguyen, Masayuki Noguchi, Tatsuya Atsumi, Blake M. Warner, John A. Chiorini
    Journal of Clinical Investigation, American Society for Clinical Investigation, 2022年03月15日, [筆頭著者]
    研究論文(学術雑誌)
  • LAMP3 inhibits autophagy and contributes to cell death by lysosomal membrane permeabilization
    Tsutomu Tanaka, Blake M. Warner, Drew G. Michael, Hiroyuki Nakamura, Toshio Odani, Hongen Yin, Tatsuya Atsumi, Masayuki Noguchi, John, A. Chiorini
    Autophagy, 1, 19, Informa {UK} Limited, 2021年11月22日, [筆頭著者]
    英語, 研究論文(学術雑誌)
  • Lysosome-associated membrane protein 3 misexpression in salivary glands induces a Sjögren’s syndrome-like phenotype in mice
    Hiroyuki Nakamura, Tsutomu Tanaka, Thomas Pranzatelli, Youngmi Ji, Hongen Yin, Paola Perez, Sandra A Afione, Shyh-Ing Jang, Corrine Goldsmith, Chang Yu Zheng, William D Swaim, Blake M Warner, Noriyuki Hirata, Masayuki Noguchi, Tatsuya Atsumi, John A Chiorini
    Annals of the Rheumatic Diseases, 80, 8, 1031, 1039, {BMJ}, 2021年03月03日, [筆頭著者]
    英語, 研究論文(学術雑誌), ObjectivesSjögren’s syndrome (SS) is an autoimmune sialadenitis with unknown aetiology. Although extensive research implicated an abnormal immune response associated with lymphocytes, an initiating event mediated by salivary gland epithelial cell (SGEC) abnormalities causing activation is poorly characterised. Transcriptome studies have suggested alternations in lysosomal function are associated with SS, but a cause and effect linkage has not been established. In this study, we demonstrated that altered lysosome activity in SGECs by expression of lysosome-associated membrane protein 3 (LAMP3) can initiate an autoimmune response with autoantibody production and salivary dysfunction similar to SS.MethodsRetroductal cannulation of the submandibular salivary glands with an adeno-associated virus serotype 2 vector encoding LAMP3 was used to establish a model system. Pilocarpine-stimulated salivary flow and the presence of autoantibodies were assessed at several time points post-cannulation. Salivary glands from the mice were evaluated using RNAseq and histologically.ResultsFollowing LAMP3 expression, saliva flow was significantly decreased and serum anti-Ro/SSA and La/SSB antibodies could be detected in the treated mice. Mechanistically, LAMP3 expression increased apoptosis in SGECs and decreased protein expression related to saliva secretion. Analysis of RNAseq data suggested altered lysosomal function in the transduced SGECs, and that the cellular changes can chemoattract immune cells into the salivary glands. Immune cells were activated via toll-like receptors by damage-associated molecular patterns released from LAMP3-expressing SGECs.ConclusionsThese results show a critical role for lysosomal trafficking in the development of SS and establish a causal relationship between LAMP3 misexpression and the development of SS.
  • Rescue of Adeno-Associated Virus Production by shRNA Cotransfection
    Maria C. Guimaro, Sandra A. Afione, Tsutomu Tanaka, John A. Chiorini
    Human Gene Therapy, 31, 19-20, 1068, 1073, Mary Ann Liebert Inc, 2020年10月01日
    英語, 研究論文(学術雑誌)
  • LAMP3 induces apoptosis and autoantigen release in Sjögren’s syndrome patients
    Tsutomu Tanaka, Blake M. Warner, Toshio Odani, Youngmi Ji, Ying-Qian Mo, Hiroyuki Nakamura, Shyh-Ing Jang, Hongen Yin, Drew G. Michael, Noriyuki Hirata, Futoshi Suizu, Satoko Ishigaki, Fabiola Reis Oliveira, Ana Carolina F. Motta, Alfredo Ribeiro-Silva, Eduardo M. Rocha, Tatsuya Atsumi, Masayuki Noguchi, John A. Chiorini
    Scientific Reports, 10, 1, 15169, 15169, Springer Science and Business Media {LLC}, 2020年09月16日, [筆頭著者], [国際誌]
    英語, 研究論文(学術雑誌), AbstractPrimary Sjögren’s syndrome (pSS) is a complex autoimmune disease characterized by dysfunction of secretory epithelia with only palliative therapy. Patients present with a constellation of symptoms, and the diversity of symptomatic presentation has made it difficult to understand the underlying disease mechanisms. In this study, aggregation of unbiased transcriptome profiling data sets of minor salivary gland biopsies from controls and Sjögren’s syndrome patients identified increased expression of lysosome-associated membrane protein 3 (LAMP3/CD208/DC-LAMP) in a subset of Sjögren’s syndrome cases. Stratification of patients based on their clinical characteristics suggested an association between increased LAMP3 expression and the presence of serum autoantibodies including anti-Ro/SSA, anti-La/SSB, anti-nuclear antibodies. In vitro studies demonstrated that LAMP3 expression induces epithelial cell dysfunction leading to apoptosis. Interestingly, LAMP3 expression resulted in the accumulation and release of intracellular TRIM21 (one component of SSA), La (SSB), and α-fodrin protein, common autoantigens in Sjögren’s syndrome, via extracellular vesicles in an apoptosis-independent mechanism. This study defines a clear role for LAMP3 in the initiation of apoptosis and an independent pathway for the extracellular release of known autoantigens leading to the formation of autoantibodies associated with this disease.ClinicalTrials.gov Identifier: NCT00001196, NCT00001390, NCT02327884.
  • Autophagy as a modulator of cell death machinery
    Masayuki Noguchi, Noriyuki Hirata, Tsutomu Tanaka, Futoshi Suizu, Hiroshi Nakajima, John, A. Chiorini
    Cell Death & Disease, 11, 7, Springer Science and Business Media {LLC}, 2020年07月08日
    英語, 研究論文(学術雑誌), AbstractThe balance between cell death and survival is a critical parameter in the regulation of cells and the maintenance of homeostasis in vivo. Three major mechanisms for cell death have been identified in mammalian cells: apoptosis (type I), autophagic cell death (type II), and necrosis (type III). These three mechanisms have been suggested to engage in cross talk with each other. Among them, autophagy was originally characterized as a cell survival mechanism for amino acid recycling during starvation. Whether autophagy functions primarily in cell survival or cell death is a critical question yet to be answered. Here, we present a comprehensive review of the cell death-related events that take place during autophagy and their underlying mechanisms in cancer and autoimmune disease development.
  • Identification of RNA aptamer which specifically interacts with PtdIns(3)P
    Thoria Donia, Bala Jyoti, Futoshi Suizu, Noriyuki Hirata, Tsutomu Tanaka, Satoko Ishigaki, Pranzatelli Thomas J. F, Junko Nio-Kobayashi, Toshihiko Iwanaga, John A. Chiorini, Masayuki Noguchi
    Biochemical and Biophysical Research Communications, 517, 1, 146, 154, Elsevier {BV}, 2019年07月24日, [国際誌]
    英語, 研究論文(学術雑誌), The phosphinositide PtdIns(3)P plays an important role in autophagy; however, the detailed mechanism of its activity remains unclear. Here, we used a Systematic Evolution of Ligands by EXponential enrichment (SELEX) screening approach to identify an RNA aptamer of 40 nucleotides that specifically recognizes and binds to intracellular lysosomal PtdIns(3)P. Binding occurs in a magnesium concentration- and pH-dependent manner, and consequently inhibits autophagy as determined by LC3II/I conversion, p62 degradation, formation of LC3 puncta, and lysosomal accumulation of Phafin2. These effects in turn inhibited lysosomal acidification, and the subsequent hydrolytic activity of cathepsin D following induction of autophagy. Given the essential role of PtdIns(3)P as a key targeting molecule for autophagy induction, identification of this novel PtdIns(3)P RNA aptamer provides new opportunities for investigating the biological functions and mechanisms of phosphoinositides.
  • Functional characterization of lysosomal interaction of Akt with VRK2
    Noriyuki Hirata, Futoshi Suizu, Mami Matsuda-Lennikov, Tsutomu Tanaka, Tatsuma Edamura, Satoko Ishigaki, Thoria Donia, Pathrapol Lithanatudom, Chikashi Obuse, Toshihiko Iwanaga, Masayuki Noguchi
    Oncogene, 37, 40, 5367, 5386, Springer Science and Business Media {LLC}, 2018年10月
    英語, 研究論文(学術雑誌)
  • Cancer-associated oxidoreductase ERO1-α promotes immune escape through up-regulation of PD-L1 in human breast cancer
    Tsutomu Tanaka, Goro Kutomi, Toshimitsu Kajiwara, Kazuharu Kukita, Vitaly Kochin, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Yoshiharu Okamoto, Koichi Hirata, Noriyuki Sato, Yasuaki Tamura
    Oncotarget, 8, 15, 24706, 24718, Impact Journals, {LLC}, 2017年04月11日, [筆頭著者]
    英語, 研究論文(学術雑誌)
  • Hypoxia augments MHC class I antigen presentation via facilitation of ERO1-α-mediated oxidative folding in murine tumor cells
    Toshimitsu Kajiwara, Tsutomu Tanaka, Kazuharu Kukita, Goro Kutomi, Keita Saito, Koichi Okuya, Akari Takaya, Vitaly Kochin, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Koichi Hirata, Noriyuki Sato, Yasuaki Tamura
    European Journal of Immunology, 46, 12, 2842, 2851, Wiley, 2016年12月
    英語, 研究論文(学術雑誌)
  • Plasticity of lung cancer stem-like cells is regulated by the transcription factor HOXA5 that is induced by oxidative stress
    Hiroshi Saijo, Yoshihiko Hirohashi, Toshihiko Torigoe, Ryota Horibe, Akari Takaya, Aiko Murai, Terufumi Kubo, Toshimitsu Kajiwara, Tsutomu Tanaka, Yosuke Shionoya, Eri Yamamoto, Reo Maruyama, Munehide Nakatsugawa, Takayuki Kanaseki, Tomohide Tsukahara, Yasuaki Tamura, Yasushi Sasaki, Takashi Tokino, Hiromu Suzuki, Toru Kondo, Hiroki Takahashi, Noriyuki Sato
    Oncotarget, 7, 31, 50043, 50056, Impact Journals, {LLC}, 2016年08月02日
    英語, 研究論文(学術雑誌)
  • Phosphorylation‐dependent Akt–Inversin interaction at the basal body of primary cilia
    Futoshi Suizu, Noriyuki Hirata, Kohki Kimura, Tatsuma Edamura, Tsutomu Tanaka, Satoko Ishigaki, Thoria Donia, Hiroko Noguchi, Toshihiko Iwanaga, Masayuki Noguchi
    The EMBO Journal, 35, 12, 1346, 1363, {EMBO}, 2016年06月15日, [国際誌]
    英語, 研究論文(学術雑誌), A primary cilium is a microtubule-based sensory organelle that plays an important role in human development and disease. However, regulation of Akt in cilia and its role in ciliary development has not been demonstrated. Using yeast two-hybrid screening, we demonstrate that Inversin (INVS) interacts with Akt. Mutation in the INVS gene causes nephronophthisis type II (NPHP2), an autosomal recessive chronic tubulointerstitial nephropathy. Co-immunoprecipitation assays show that Akt interacts with INVS via the C-terminus. In vitro kinase assays demonstrate that Akt phosphorylates INVS at amino acids 864-866 that are required not only for Akt interaction, but also for INVS dimerization. Co-localization of INVS and phosphorylated form of Akt at the basal body is augmented by PDGF-AA Akt-null MEF cells as well as siRNA-mediated inhibition of Akt attenuated ciliary growth, which was reversed by Akt reintroduction. Mutant phosphodead- or NPHP2-related truncated INVS, which lack Akt phosphorylation sites, suppress cell growth and exhibit distorted lumen formation and misalignment of spindle axis during cell division. Further studies will be required for elucidating functional interactions of Akt-INVS at the primary cilia for identifying the molecular mechanisms underlying NPHP2.
  • Cancer-associated oxidoreductase ERO1-α drives the production of VEGF via oxidative protein folding and regulating the mRNA level
    Tsutomu Tanaka, Goro Kutomi, Toshimitsu Kajiwara, Kazuharu Kukita, Vitaly Kochin, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Yoshiharu Okamoto, Koichi Hirata, Noriyuki Sato, Yasuaki Tamura
    British Journal of Cancer, 114, 11, 1227, 1234, Springer Science and Business Media {LLC}, 2016年05月24日, [筆頭著者, 責任著者]
    英語, 研究論文(学術雑誌)
  • Primary Cilium-Mediated Crosstalk of Signaling Cascades in Ciliogenesis: Implications for Tumorigenesis and Senescence
    Tsutomu Tanaka
    Cell Communication Insights, 8, 13, 24, Portico, 2016年05月19日
    研究論文(学術雑誌)
  • Liposomally formulated phospholipid-conjugated indocyanine green for intra-operative brain tumor detection and resection
    Akiko Suganami, Yasuo Iwadate, Sayaka Shibata, Masamichi Yamashita, Tsutomu Tanaka, Natsuki Shinozaki, Ichio Aoki, Naokatsu Saeki, Hiroshi Shirasawa, Yoshiharu Okamoto, Yutaka Tamura
    International Journal of Pharmaceutics, 496, 2, 401, 406, Elsevier {BV}, 2015年12月30日
    英語, 研究論文(学術雑誌)
  • CpG-A stimulates Hsp72 secretion from plasmacytoid dendritic cells, facilitating cross-presentation
    Tsutomu Tanaka, Toshimitsu Kajiwara, Goro Kutomi, Takehiro Kurotaki, Keita Saito, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Koichi Hirata, Yoshiharu Okamoto, Noriyuki Sato, Yasuaki Tamura
    Immunology Letters, 167, 1, 34, 40, Elsevier {BV}, 2015年09月, [筆頭著者]
    英語, 研究論文(学術雑誌)
  • Cancer-Associated Oxidase ERO1-α Regulates the Expression of MHC Class I Molecule via Oxidative Folding
    Kazuharu Kukita, Yasuaki Tamura, Tsutomu Tanaka, Toshimitsu Kajiwara, Goro Kutomi, Keita Saito, Koichi Okuya, Akari Takaya, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Tomohisa Furuhata, Koichi Hirata, Noriyuki Sato
    The Journal of Immunology, 194, 10, 4988, 4996, The American Association of Immunologists, 2015年05月15日
    英語, 研究論文(学術雑誌)
  • Cancer-Associated Oxidoreductase ERO1-α Drives the Production of Tumor-Promoting Myeloid-Derived Suppressor Cells via Oxidative Protein Folding
    Tsutomu Tanaka, Toshimitsu Kajiwara, Toshihiko Torigoe, Yoshiharu Okamoto, Noriyuki Sato, Yasuaki Tamura
    The Journal of Immunology, 194, 4, 2004, 2010, The American Association of Immunologists, 2015年02月15日, [筆頭著者]
    英語, 研究論文(学術雑誌)
  • Heat shock protein 90 targets a chaperoned peptide to the static early endosome for efficient cross‐presentation by human dendritic cells
    Tsutomu Tanaka, Koichi Okuya, Goro Kutomi, Akari Takaya, Toshimitsu Kajiwara, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Koichi Hirata, Yoshiharu Okamoto, Noriyuki Sato, Yasuaki Tamura
    Cancer Science, 106, 1, 18, 24, Wiley, 2015年01月, [筆頭著者]
    英語, 研究論文(学術雑誌)
  • 過剰発現した小胞体ジスルフィド・オキシターゼ1-α(ERO1-α)は抗腫瘍免疫応答を抑制する(Enhanced expression of endoplasmic reticulum disulfide oxidase 1-α(ERO1-α) inhibits anti-tumor immune response)               
    田中 努, 田村 保明, 久木田 和晴, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    日本癌学会総会記事, 72回, 155, 155, (一社)日本癌学会, 2013年10月
    英語
  • Human endoplasmic reticulum oxidoreductin 1-α is a novel predictor for poor prognosis of breast cancer
    Goro Kutomi, Yasuaki Tamura, Tsutomu Tanaka, Toshimitsu Kajiwara, Kazuharu Kukita, Tousei Ohmura, Hiroaki Shima, Tomoko Takamaru, Fukino Satomi, Yasuyo Suzuki, Toshihiko Torigoe, Noriyuki Sato, Koichi Hirata
    Cancer Science, 104, 8, 1091, 1096, Wiley, 2013年08月
    英語, 研究論文(学術雑誌)

講演・口頭発表等

  • The regulation of MHC-I antigen presentation pathway by cooperation of NLRC5 and IRF1.               
    Tsutomu Tanaka, Torsten B. Meissner, Saptha Vijayan, Kyoung-Hee Lee, Yuen-Joyce Liu, Isaac Downs, Jason Yeung, Koichi S. Kobayashi
    19th International Congress of Immunology (IUIS), 2025年, ポスター発表
    2025年08月17日 - 2025年08月22日
  • Kras変異非小細胞肺癌の免疫逃避メカニズムの解明               
    田中 努, Steven Cho, 渡邊 俊之, 小田 義崇, Xin Sun, 吉濱 小百合, Suhail Yousuf, Tabasum Sidi, 田中 伸哉, 小林 弘一
    第114回日本病理学会総会, 2025年
  • Role of MHC class I in lung cancer with Kras mutation in the development.               
    Tsutomu Tanaka, Sayuri Yoshihama, Suhail Yousuf, Tabasum Sidiq, Yusuke Kasuga, Atsuki Takeishi, Yoshitaka Oda, Steven Cho, Shinya Tanaka, Koichi Kobayashi
    第53回日本免疫学会学術集会, 2024年
    2024年, [招待講演]
  • Increased expression of lysosomal associated membrane protein (LAMP) 3 in the salivary glands of Sjögren’s syndrome patients can stimulate stalled autophagy and apoptosis.               
    Tsutomu Tanaka, Blake M. Warner, Toshio Odani, Hongen Yin, Tatsuya Atsumi, Masayuki Noguchi, John A. Chiorini
    The 14th International Sjögren’s Syndrome Symposium, 2018年04月, ポスター発表
    2018年04月
  • 腫瘍高発現性酸化酵素ERO1-αはEMTを調節し肺転移を制御する               
    田中 努, 田村 保明, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第10回日本臨床ストレス応答学会大会, 2015年11月, 口頭発表(一般)
    2015年11月
  • Cancer specific oxidase ERO1-α promotes the immune escape via up-regulation of PD-L1.               
    田中 努, 田村 保明, 梶原 敏充, 九冨 五郎, 鳥越 俊彦, 岡本 芳晴, 平田 公一, 佐藤 昇志
    第74回日本癌学会総会, 2015年10月, 口頭発表(一般)
    2015年10月
  • Enhanced expression of ERO1-α within tumors regulates the condition for tumor growth in vivo.               
    田中 努, 田村 保明, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第104回日本病理学会総会, 2015年04月, 口頭発表(一般)
    2015年04月
  • 腫瘍に高発現する酸化酵素ERO1-αは、腫瘍増殖環境を整える               
    田中 努, 田村 保明, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第9回日本臨床ストレス応答学会大会, 2014年11月, 口頭発表(一般)
    2014年11月
  • Enhanced expression of endoplasmic reticulum oxidoreductin 1-α (ERO1-α) promotes tumor growth and pulmonary metastasis.               
    田中 努, 田村 保明, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第73回日本癌学会総会, 2014年09月, ポスター発表
    2014年09月
  • 腫瘍に高発現する酸化酵素ERO1-αは癌幹細胞形質の維持に関与する               
    田中 努, 田村 保明, 久木田 和晴, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第103回日本病理学会総会, 2014年04月, 口頭発表(一般)
    2014年04月
  • Enhanced expression of endoplasmic reticulum disulfide oxidase 1-α (ERO1-α) inhibits anti-tumor immune response.               
    田中 努, 田村 保明, 久木田 和晴, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第72回日本癌学会総会, 2013年10月, 口頭発表(一般)
    2013年10月
  • 腫瘍に高発現する酸化酵素ERO1-αは、抗腫瘍免疫応答を抑制する               
    田中 努, 田村 保明, 久木田 和晴, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第102回日本病理学会総会, 2013年06月, 口頭発表(一般)
    2013年06月

所属学協会

  • 2015年 - 現在
    日本免疫学会               
  • 2013年 - 現在
    日本病理学会               
  • 2012年 - 現在
    日本癌学会               

共同研究・競争的資金等の研究課題

  • 新規NLRC5結合タンパク質を介したMHC-I依存的免疫制御機構の解明
    科学研究費助成事業
    2025年04月 - 2028年03月
    田中 努
    日本学術振興会, 基盤研究(C), 北海道大学, 研究代表者, 25K10418
  • MHCクラスI誘導技術を用いた新規膀胱癌免疫療法の開発
    科学研究費助成事業
    2025年04月 - 2028年03月
    小林 弘一, 田中 努, 竹石 惇樹, 春日 優介
    日本学術振興会, 基盤研究(B), 北海道大学, 25K02512
  • 免疫チェックポイント阻害剤耐性皮膚癌に対するMHCクラスI誘導技術を用いた新規免疫療法の開発               
    次世代がん医療加速化研究事業
    2024年10月 - 2026年03月
    小林弘一, 田中伸哉, 田中努
    国立研究開発法人日本医療研究開発機構, 北海道大学 医学研究院, 研究分担者
  • 選択的MHC発現誘導機構の解明と癌免疫への応用
    科学研究費助成事業
    2023年08月31日 - 2025年03月31日
    田中 努
    日本学術振興会, 研究活動スタート支援, 北海道大学, 23K19476
  • エピゲノム編集を用いた新規肺癌免疫療法の開発
    科学研究費助成事業
    2023年06月30日 - 2025年03月31日
    小林 弘一, 田中 努
    日本学術振興会, 挑戦的研究(萌芽), 北海道大学, 23K18207
  • MHC-I 転写活性化因子NLRC5のCOVID-19における役割
    科学研究費助成事業
    2022年04月01日 - 2025年03月31日
    小林 弘一, 澤 洋文, 田中 努, 福原 崇介, 應田 涼太
    日本学術振興会, 基盤研究(B), 北海道大学, 23K24145
  • MHC-I 転写活性化因子NLRC5のCOVID-19における役割
    科学研究費助成事業
    2022年04月 - 2025年03月
    小林 弘一, 澤 洋文, 福原 崇介, 田中 努, 應田 涼太
    日本学術振興会, 基盤研究(B), 北海道大学, 研究分担者, 22H02883
  • Kras変異肺がんにおけるMHC class I 発現低下と浸潤免疫細胞の役割               
    2024年若手免疫学研究推進事業
    2024年01月 - 2024年12月
    田中努
    日本免疫学会, 北海道大学大学院医学研究院, 研究代表者
  • 新規MHCクラスI発現制御因子の発見とその解析               
    創成若手研究加速事業
    2023年06月 - 2024年03月
    北海道大学, 研究代表者