Updated on 2026/03/27

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写真a

 
Tatsuma Ban
 
Organization
Graduate School of Medicine Department of Medicine Immunology Lecturer
School of Medicine Medical Course
Title
Lecturer
Homepage
http://www-user.yokohama-cu.ac.jp/~immunol/
Profile

自己免疫疾患や自己炎症性疾患の病態理解と新規治療法開発に向けた基礎医学研究を行っています。指定難病である全身性エリテマトーデス（SLE）、特発性拡張型心筋症（DCM）、ならびに新しい自己炎症性疾患であるVEXAS症候群を主な研究対象疾患としています。SLEでは治療標的として転写因子であるIRF5に着目して研究開発を進めています。

External link

Degree

  • 博士(医学) ( 東京大学 )

Research Interests

  • 転写因子

  • 自己免疫疾患

  • 自然免疫応答

  • 自己炎症性疾患

Research Areas

  • Life Science / Immunology

Education

  • The University of Tokyo   Graduate School of Medicine   Pathology, Immunology and Microbiology

    2008.4 - 2012.3

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  • The University of Tokyo   Graduate School of Medicine

    2006.4 - 2008.3

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  • The University of Tokyo

    2002.4 - 2006.3

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Research History

  • Yokohama City University   Lecturer

    2022.4

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  • Yokohama City University   Assistant Professor

    2013.4 - 2022.3

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  • Yokohama City University

    2012.4 - 2013.3

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Professional Memberships

  • 日本インターフェロン・サイトカイン学会

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  • THE JAPANESE SOCIETY FOR IMMUNOLOGY

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  • THE MOLECULAR BIOLOGY SOCIETY OF JAPAN

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  • International Cytokine & Interferon Society

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Papers

  • cGAS-IFN-I responses by extracting nuclear DNA from dying cells via nucleocytosis. Reviewed International journal

    Hideo Negishi, Yusuke Wada, Yoshitaka Shirasaki, Tomoya Hayashi, Yuji Kubota, Tomio Iwasaki, Mina Kurosawa, Tatsuma Ban, Daisuke Muto, Yusuke Suenaga, Taichi Kojima, Yuzuki Matsuda, Sean Lord Irish, Kosuke Dodo, Toru Suzuki, Mai Yamagishi, Burcu Temizoz, Atsushi Yoshimori, Chisato Kanai, Yoji Nagasaki, Masaki Ohmuraya, Tomohiko Tamura, Atsushi Iwama, Toshifumi Inada, Etsushi Kuroda, Kouji Kobiyama, Noriko Toyama-Sorimachi, Mutsuhiro Takekawa, Cevayir Coban, Ken J Ishii

    Nature communications   17 ( 1 )   1658 - 1658   2026.2

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    Self-DNA triggers cGAS-STING-mediated type I interferon (IFN-I) to induce both protective and pathogenic immune responses; however, how self-DNA activates the cytosolic cGAS-STING pathway remains unclear. Here we show that the cGAS/STING/IFN-I axis is activated by self-DNA via a process termed 'nucleocytosis', in which nuclear DNA is extracted from dying cells by macrophages. Mechanistically, lysosomal malfunction, via both proton loss and palmitoyl-protein thioesterase 1 (PPT1) inhibition, triggers cell death and calreticulin accumulation in the nuclei. Live-cell imaging of secretion activity reveals that macrophages access the calreticulin-enriched nuclei of dying cells and extract DNA for cGAS-STING activation. Consistent with these findings, PPT1-targeting cationic amphiphilic drugs induce a cGAS-STING-dependent IFN-I response in vitro and in vivo. Our findings thus identify nucleocytosis as a macrophage function for nuclear DNA extraction and induction of the cGAS/IFN-I axis, and suggest that nucleocytosis-inducing cell death could be a druggable target for treating self-DNA-related inflammatory diseases.

    DOI： 10.1038/s41467-026-68839-w

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  • Innate type 2 lymphocytes trigger an inflammatory switch in alveolar macrophages. Reviewed International journal

    Stijn Verwaerde, Jean-François Hastir, Sjoerd T T Schetters, Ursula Smole, Leen Seys, Antonio P Baptista, Kieran English, Martijn J Schuijs, Helena Aegerter, Karel F A Van Damme, Aimée Bugler-Lamb, Nikita Gerebtsov, Wendy Toussaint, Tatsuma Ban, Tomohiko Tamura, Florent Ginhoux, Zhaoyuan Liu, Wouter Saelens, Hamida Hammad, Martin Guilliams, Bart N Lambrecht

    Immunity   59 ( 1 )   60 - 78   2026.1

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    Tissue-resident alveolar macrophages (trAMs) safeguard gas exchange by restraining inflammation. Compared with recruited alveolar macrophages (recAMs), trAMs are considered more immunoregulatory and resilient to inflammatory reprogramming. Using a mouse model enabling selective trAM depletion and replacement, we uncovered a pro-inflammatory role for trAMs during type 2 immunity. Upon allergen exposure, interleukin-33-activated innate type 2 lymphoid cells (ILC2s) produced interleukin-13, which reprogrammed trAMs through induction of the transcription factor interferon regulatory factor 4 (IRF4). IRF4 suppressed the expression of the transcription factor peroxisome proliferator-activated receptor gamma (PPARγ) and dismantled the PPARγ-dependent homeostatic regulon that defines trAM identity, while initiating a transcriptional program driving chemokine production and cell fusion. This resulted in the recruitment of granulocytes, ILC2s, and regulatory T cells, as well as the formation of multinucleated giant cells in the alveolar niche. Thus, a PPARγ-to-IRF4 switch reconfigures trAMs into pro-inflammatory effectors, promoting allergen-induced lung pathology.

    DOI： 10.1016/j.immuni.2025.11.015

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  • Physical and functional interaction among Irf8 enhancers during dendritic cell differentiation Reviewed

    Takaya Yamasaki, Akira Nishiyama, Nagomi Kurogi, Koutarou Nishimura, Shion Nishida, Daisuke Kurotaki, Tatsuma Ban, Jordan A. Ramilowski, Keiko Ozato, Atsushi Toyoda, Tomohiko Tamura

    Cell Reports   43 ( 4 )   114107 - 114107   2024.4

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    Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    DOI： 10.1016/j.celrep.2024.114107

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  • Machine learning for prediction of immunotherapeutic outcome in non-small-cell lung cancer based on circulating cytokine signatures. Reviewed International journal

    Feifei Wei, Koichi Azuma, Yoshiro Nakahara, Haruhiro Saito, Norikazu Matsuo, Tomoyuki Tagami, Taku Kouro, Yuka Igarashi, Takaaki Tokito, Terufumi Kato, Tetsuro Kondo, Shuji Murakami, Ryo Usui, Hidetomo Himuro, Shun Horaguchi, Kayoko Tsuji, Kenta Murotani, Tatsuma Ban, Tomohiko Tamura, Yohei Miyagi, Tetsuro Sasada

    Journal for immunotherapy of cancer   11 ( 7 )   2023.7

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    BACKGROUND: Immune checkpoint inhibitor (ICI) therapy has substantially improved the overall survival (OS) in patients with non-small-cell lung cancer (NSCLC); however, its response rate is still modest. In this study, we developed a machine learning-based platform, namely the Cytokine-based ICI Response Index (CIRI), to predict the ICI response of patients with NSCLC based on the peripheral blood cytokine profiles. METHODS: We enrolled 123 and 99 patients with NSCLC who received anti-PD-1/PD-L1 monotherapy or combined chemotherapy in the training and validation cohorts, respectively. The plasma concentrations of 93 cytokines were examined in the peripheral blood obtained from patients at baseline (pre) and 6 weeks after treatment (early during treatment: edt). Ensemble learning random survival forest classifiers were developed to select feature cytokines and predict the OS of patients undergoing ICI therapy. RESULTS: Fourteen and 19 cytokines at baseline and on treatment, respectively, were selected to generate CIRI models (namely preCIRI14 and edtCIRI19), both of which successfully identified patients with worse OS in two completely independent cohorts. At the population level, the prediction accuracies of preCIRI14 and edtCIRI19, as indicated by the concordance indices (C-indices), were 0.700 and 0.751 in the validation cohort, respectively. At the individual level, patients with higher CIRI scores demonstrated worse OS [hazard ratio (HR): 0.274 and 0.163, and p<0.0001 and p=0.0044 in preCIRI14 and edtCIRI19, respectively]. By including other circulating and clinical features, improved prediction efficacy was observed in advanced models (preCIRI21 and edtCIRI27). The C-indices in the validation cohort were 0.764 and 0.757, respectively, whereas the HRs of preCIRI21 and edtCIRI27 were 0.141 (p<0.0001) and 0.158 (p=0.038), respectively. CONCLUSIONS: The CIRI model is highly accurate and reproducible in determining the patients with NSCLC who would benefit from anti-PD-1/PD-L1 therapy with prolonged OS and may aid in clinical decision-making before and/or at the early stage of treatment.

    DOI： 10.1136/jitc-2023-006788

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  • Genetic and chemical inhibition of IRF5 suppresses pre-existing mouse lupus-like disease Reviewed International journal

    Tatsuma Ban, Masako Kikuchi, Go R. Sato, Akio Manabe, Noriko Tagata, Kayo Harita, Akira Nishiyama, Kenichi Nishimura, Ryusuke Yoshimi, Yohei Kirino, Hideyuki Yanai, Yoshiko Matsumoto, Shuichi Suzuki, Hiroe Hihara, Masashi Ito, Kappei Tsukahara, Kentaro Yoshimatsu, Tadashi Yamamoto, Tadatsugu Taniguchi, Hideaki Nakajima, Shuichi Ito, Tomohiko Tamura

    Nature Communications   12 ( 1 )   4379 - 4379   2021.7

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    Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

    <title>Abstract</title>The transcription factor IRF5 has been implicated as a therapeutic target for the autoimmune disease systemic lupus erythematosus (SLE). However, IRF5 activation status during the disease course and the effects of IRF5 inhibition after disease onset are unclear. Here, we show that SLE patients in both the active and remission phase have aberrant activation of IRF5 and interferon-stimulated genes. Partial inhibition of IRF5 is superior to full inhibition of type I interferon signaling in suppressing disease in a mouse model of SLE, possibly due to the function of IRF5 in oxidative phosphorylation. We further demonstrate that inhibition of IRF5 via conditional <italic>Irf5</italic> deletion and a newly developed small-molecule inhibitor of IRF5 after disease onset suppresses disease progression and is effective for maintenance of remission in mice. These results suggest that IRF5 inhibition might overcome the limitations of current SLE therapies, thus promoting drug discovery research on IRF5 inhibitors.

    DOI： 10.1038/s41467-021-24609-4

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    Other Link： http://www.nature.com/articles/s41467-021-24609-4

  • A RUNX–CBFβ-driven enhancer directs the Irf8 dose-dependent lineage choice between DCs and monocytes Reviewed International journal

    Koichi Murakami, Haruka Sasaki, Akira Nishiyama, Daisuke Kurotaki, Wataru Kawase, Tatsuma Ban, Jun Nakabayashi, Satoko Kanzaki, Yoichi Sekita, Hideaki Nakajima, Keiko Ozato, Tohru Kimura, Tomohiko Tamura

    Nature Immunology   22 ( 3 )   301 - 311   2021.3

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    The transcription factor IRF8 is essential for the development of monocytes and dendritic cells (DCs), whereas it inhibits neutrophilic differentiation. It is unclear how Irf8 expression is regulated and how this single transcription factor supports the generation of both monocytes and DCs. Here, we identified a RUNX-CBFβ-driven enhancer 56 kb downstream of the Irf8 transcription start site. Deletion of this enhancer in vivo significantly decreased Irf8 expression throughout the myeloid lineage from the progenitor stages, thus resulting in loss of common DC progenitors and overproduction of Ly6C+ monocytes. We demonstrated that high, low or null expression of IRF8 in hematopoietic progenitor cells promotes differentiation toward type 1 conventional DCs, Ly6C+ monocytes or neutrophils, respectively, via epigenetic regulation of distinct sets of enhancers in cooperation with other transcription factors. Our results illustrate the mechanism through which IRF8 controls the lineage choice in a dose-dependent manner within the myeloid cell system.

    DOI： 10.1038/s41590-021-00871-y

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    Other Link： http://www.nature.com/articles/s41590-021-00871-y

  • Regulation and role of the transcription factor IRF5 in innate immune responses and systemic lupus erythematosus Reviewed International journal

    Tatsuma Ban, Go R Sato, Tomohiko Tamura

    International Immunology   30 ( 11 )   529 - 536   2018.5

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    Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Oxford University Press (OUP)  

    The transcription factor interferon regulatory factor-5 (IRF5) plays an important role in innate immune responses via the TLR-MyD88 (Toll-like receptor - myeloid differentiation primary response 88) pathway. IRF5 is also involved in the pathogenesis of the autoimmune disease systemic lupus erythematosus (SLE). Recent studies have identified new regulators, both positive and negative, which act on IRF5 activation events in the TLR-MyD88 pathway such as post-translational modifications, dimerization and nuclear translocation. A model of the causal relationship between IRF5 activation and SLE pathogenesis proposes that a loss of the negative regulation of IRF5 causes its hyperactivation, resulting in hyperproduction of type I interferons and other cytokines, and ultimately in the development of SLE. Importantly, to our knowledge, all murine models of SLE studied thus far have shown that IRF5 is required for the pathogenesis of SLE-like diseases. During the development of SLE-like diseases, IRF5 plays key roles in various cell types, including dendritic cells and B cells. It is noteworthy that the onset of SLE-like diseases can be inhibited by reducing the activity or amount of IRF5 by half. Therefore, IRF5 is an important therapeutic target of SLE, and selective suppression of its activity and expression may potentially lead to the development of new therapies.

    DOI： 10.1093/intimm/dxy032

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  • Lyn Kinase Suppresses the Transcriptional Activity of IRF5 in the TLR-MyD88 Pathway to Restrain the Development of Autoimmunity Reviewed

    Tatsuma Ban, Go R. Sato, Akira Nishiyama, Ai Akiyama, Marie Takasuna, Marina Umehara, Shinsuke Suzuki, Motohide Ichino, Satoko Matsunaga, Ayuko Kimura, Yayoi Kimura, Hideyuki Yanai, Sadakazu Miyashita, Junro Kuromitsu, Kappei Tsukahara, Kentaro Yoshimatsu, Itaru Endo, Tadashi Yamamoto, Hisashi Hirano, Akihide Ryo, Tadatsugu Taniguchi, Tomohiko Tamura

    IMMUNITY   45 ( 2 )   319 - 332   2016.8

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    DOI： 10.1016/j.immuni.2016.07.015

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  • Suppression of immune responses by nonimmunogenic oligodeoxynucleotides with high affinity for high-mobility group box proteins (HMGBs) Reviewed

    Hideyuki Yanai, Shiho Chiba, Tatsuma Ban, Yukana Nakaima, Takashi Onoe, Kenya Honda, Hideki Ohdan, Tadatsugu Taniguchi

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   108 ( 28 )   11542 - 11547   2011.7

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    DOI： 10.1073/pnas.1108535108

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  • HMGB proteins function as universal sentinels for nucleic-acid-mediated innate immune responses Reviewed

    Hideyuki Yanai, Tatsuma Ban, ZhiChao Wang, Myoung Kwon Choi, Takeshi Kawamura, Hideo Negishi, Makoto Nakasato, Yan Lu, Sho Hangai, Ryuji Koshiba, David Savitsky, Lorenza Ronfani, Shizuo Akira, Marco E. Bianchi, Kenya Honda, Tomohiko Tamura, Tatsuhiko Kodama, Tadatsugu Taniguchi

    NATURE   462 ( 7269 )   99 - U110   2009.11

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    DOI： 10.1038/nature08512

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  • DAI (DLM-1/ZBP1) is a cytosolic DNA sensor and an activator of innate immune response Reviewed

    Akinori Takaoka, ZhiChao Wang, Myoung Kwon Choi, Hideyuki Yanai, Hideo Negishi, Tatsuma Ban, Yan Lu, Makoto Miyagishi, Tatsuhiko Kodama, Kenya Honda, Yusuke Ohba, Tadatsugu Taniguchi

    NATURE   448 ( 7152 )   501 - U14   2007.7

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    DOI： 10.1038/nature06013

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  • Predictive value of interferon regulatory factor 5 nuclear translocation in B cells for disease activity and flare in systemic lupus erythematosus: a prospective observational cohort study. Reviewed International journal

    Yoshiro Kanayama, Tatsuma Ban, Go R Sato, Yoshiyuki Arinuma, Yu Matsueda, Kunihiro Yamaoka, Tomohiko Tamura

    Modern rheumatology   2026.3

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

    OBJECTIVE: This study aimed to determine whether interferon regulatory factor 5 (IRF5) activation and its temporal dynamics in immune cells correlate with disease activity and flares in patients with systemic lupus erythematosus (SLE). METHODS: Patients with SLE were prospectively enrolled and followed up for 52 weeks. The IRF5 nuclear translocation rate (NTR) was assessed in monocytes, dendritic cells, and B cells during baseline and follow-ups. Associations among IRF5 NTR, disease activity, and flares were statistically analyzed. RESULTS: Of 40 patients enrolled, 27 were included in the analysis after meeting all inclusion criteria. Baseline IRF5 NTR in B cells was correlated with SLE disease activity index scores (r = 0.529, p = 0.005). Nineteen patients developed flares, and high baseline IRF5 NTR showed good predictive accuracy (AUC = 0.763) and an increased flare risk (OR = 25.5, p = 0.003). In survival analysis, patients with high IRF5 NTR had significantly shorter flare-free survival (log-rank p = 0.030) and higher hazard of flare (HR = 7.43, p = 0.010). IRF5 NTR further increased during the 12 weeks preceding flares (p = 0.040). CONCLUSION: The IRF5 NTR in B cells is a potential biomarker for disease activity and flare prediction in SLE.

    DOI： 10.1093/mr/roag024

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  • Multi-omics analysis-based clinical and functional significance of a novel prognostic and immunotherapeutic gene signature derived from amino acid metabolism pathways in lung adenocarcinoma. International journal

    Huihui Xiang, Rika Kasajima, Koichi Azuma, Tomoyuki Tagami, Asami Hagiwara, Yoshiro Nakahara, Haruhiro Saito, Yuka Igarashi, Feifei Wei, Tatsuma Ban, Mitsuyo Yoshihara, Yoshiyasu Nakamura, Shinya Sato, Shiro Koizume, Tomohiko Tamura, Tetsuro Sasada, Yohei Miyagi

    Frontiers in immunology   15   1361992 - 1361992   2024

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    BACKGROUND: Studies have shown that tumor cell amino acid metabolism is closely associated with lung adenocarcinoma (LUAD) development and progression. However, the comprehensive multi-omics features and clinical impact of the expression of genes associated with amino acid metabolism in the LUAD tumor microenvironment (TME) are yet to be fully understood. METHODS: LUAD patients from The Cancer Genome Atlas (TCGA) database were enrolled in the training cohort. Using least absolute shrinkage and selection operator Cox regression analysis, we developed PTAAMG-Sig, a signature based on the expression of tumor-specific amino acid metabolism genes associated with overall survival (OS) prognosis. We evaluated its predictive performance for OS and thoroughly explored the effects of the PTAAMG-Sig risk score on the TME. The risk score was validated in two Gene Expression Omnibus (GEO) cohorts and further investigated against an original cohort of chemotherapy combined with immune checkpoint inhibitors (ICIs). Somatic mutation, chemotherapy response, immunotherapy response, gene set variation, gene set enrichment, immune infiltration, and plasma-free amino acids (PFAAs) profile analyses were performed to identify the underlying multi-omics features. RESULTS: TCGA datasets based PTAAMG-Sig model consisting of nine genes, KYNU, PSPH, PPAT, MIF, GCLC, ACAD8, TYRP1, ALDH2, and HDC, could effectively stratify the OS in LUAD patients. The two other GEO-independent datasets validated the robust predictive power of PTAAMG-Sig. Our differential analysis of somatic mutations in the high- and low-risk groups in TCGA cohort showed that the TP53 mutation rate was significantly higher in the high-risk group and negatively correlated with OS. Prediction from transcriptome data raised the possibility that PTAAMG-Sig could predict the response to chemotherapy and ICIs therapy. Our immunotherapy cohort confirmed the predictive ability of PTAAMG-Sig in the clinical response to ICIs therapy, which correlated with the infiltration of immune cells (e.g., T lymphocytes and nature killer cells). Corresponding to the concentrations of PFAAs, we discovered that the high PTAAMG-Sig risk score patients showed a significantly lower concentration of plasma-free α-aminobutyric acid. CONCLUSION: In patients with LUAD, the PTAAMG-Sig effectively predicted OS, drug sensitivity, and immunotherapy outcomes. These findings are expected to provide new targets and strategies for personalized treatment of LUAD patients.

    DOI： 10.3389/fimmu.2024.1361992

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  • Irf5 siRNA-loaded biodegradable lipid nanoparticles ameliorate concanavalin A-induced liver injury Reviewed

    Wataru Kawase, Daisuke Kurotaki, Yuta Suzuki, Hiroshi Ishihara, Tatsuma Ban, Go R. Sato, Juri Ichikawa, Hideyuki Yanai, Tadatsugu Taniguchi, Kappei Tsukahara, Tomohiko Tamura

    Molecular Therapy - Nucleic Acids   25   708 - 715   2021.9

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    DOI： 10.1016/j.omtn.2021.08.023

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  • Combining IL-6 and SARS-CoV-2 RNAaemia-based risk stratification for fatal outcomes of COVID-19. Reviewed International journal

    Ryo Saji, Mototsugu Nishii, Kazuya Sakai, Kei Miyakawa, Yutaro Yamaoka, Tatsuma Ban, Takeru Abe, Yutaro Ohyama, Kento Nakajima, Taro Hiromi, Reo Matsumura, Naoya Suzuki, Hayato Taniguchi, Tsuyoshi Otsuka, Yasufumi Oi, Fumihiro Ogawa, Munehito Uchiyama, Kohei Takahashi, Masayuki Iwashita, Yayoi Kimura, Satoshi Fujii, Ryosuke Furuya, Tomohiko Tamura, Akihide Ryo, Ichiro Takeuchi

    PloS one   16 ( 8 )   e0256022   2021

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    BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic rapidly increases the use of mechanical ventilation (MV). Such cases further require extracorporeal membrane oxygenation (ECMO) and have a high mortality. OBJECTIVE: We aimed to identify prognostic biomarkers pathophysiologically reflecting future deterioration of COVID-19. METHODS: Clinical, laboratory, and outcome data were collected from 102 patients with moderate to severe COVID-19. Interleukin (IL)-6 level and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA copy number in plasma were assessed with ELISA kit and quantitative PCR. RESULTS: Twelve patients died or required ECMO owing to acute respiratory distress syndrome despite the use of MV. Among various variables, a ratio of oxygen saturation to fraction of inspired oxygen (SpO2/FiO2), IL-6, and SARS-CoV-2 RNA on admission before intubation were strongly predictive of fatal outcomes after the MV use. Moreover, among these variables, combining SpO2/FiO2, IL-6, and SARS-CoV-2 RNA showed the highest accuracy (area under the curve: 0.934). In patients with low SpO2/FiO2 (< 261), fatal event-rate after the MV use at the 30-day was significantly higher in patients with high IL-6 (> 49 pg/mL) and SARS-CoV-2 RNAaemia (> 1.5 copies/μL) compared to those with high IL-6 or RNAaemia or without high IL-6 and RNAaemia (88% vs. 22% or 8%, log-rank test P = 0.0097 or P < 0.0001, respectively). CONCLUSIONS: Combining SpO2/FiO2 with high IL-6 and SARS-CoV-2 RNAaemia which reflect hyperinflammation and viral overload allows accurately and before intubation identifying COVID-19 patients at high risk for ECMO use or in-hospital death despite the use of MV.

    DOI： 10.1371/journal.pone.0256022

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  • Selective suppression of IRF5 activity by Lyn in the TLR-MyD88 pathway restrains the development of SLE-like disease

    Tatsuma Ban, Go Sato, Akira Nishiyama, Satoko Matsunaga, Ayuko Kimura, Yayoi Kimura, Hideyuki Yanai, Yoshiko Matsumoto, Hiroe Hihara, Tadashi Yamamoto, Hisashi Hirano, Akihide Ryo, Kappei Tsukahara, Kentaro Yoshimatsu, Tadatsugu Taniguchi, Tomohiko Tarnura

    CYTOKINE   100   69 - 69   2017.12

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  • Phos-tag Immunoblot Analysis for Detecting IRF5 Phosphorylation Reviewed International journal

    Go Sato, Tatsuma Ban, Tomohiko Tamura

    BIO-PROTOCOL   7 ( 10 )   e2295   2017

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    Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Bio-Protocol, LLC  

    While the activation of the transcription factor interferon regulatory factor 5 (IRF5) is critical for the induction of innate immune responses, it also contributes to the pathogenesis of the autoimmune disease systemic lupus erythematosus (SLE). IRF5 phosphorylation is a hallmark of its activation in the Toll-like receptor (TLR) pathway, where active IRF5 induces type I interferon and proinflammatory cytokine genes. By using the phosphate-binding molecule Phos-tag, without either radioisotopes or phospho-specific antibodies, the protocol described here enables detection of the phosphorylation of both human and murine IRF5, as well as that of other proteins.

    DOI： 10.21769/bioprotoc.2295

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  • A critical link between Lyn-mediated suppression of the TLR-MyD88-IRF5 pathway and the development of SLE-like disease

    Tatsuma Ban, Go Sato, Akira Nishiyama, Ai Akiyama, Marie Takasuna, Marina Umehara, Shinsuke Suzuki, Motohide Ichino, Satoko Matsunaga, Ayuko Kimura, Yayoi Kimura, Hideyuki Yanai, Sadakazu Miyashita, Junro Kuromitsu, Kappei Tsukahara, Kentaro Yoshimatsu, Itaru Endo, Tadashi Yamamoto, Hisashi Hirano, Akihide Ryo, Tadatsugu Taniguchi, Tomohiko Tamura

    JOURNAL OF IMMUNOLOGY   196   2016.5

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  • IRF8 inhibits C/EBPα activity to restrain mononuclear phagocyte progenitors from differentiating into neutrophils Reviewed

    Daisuke Kurotaki, Michio Yamamoto, Akira Nishiyama, Kazuhiro Uno, Tatsuma Ban, Motohide Ichino, Haruka Sasaki, Satoko Matsunaga, Masahiro Yoshinari, Akihide Ryo, Masatoshi Nakazawa, Keiko Ozato, Tomohiko Tamura

    Nature Communications   5 ( 1 )   2014.12

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    DOI： 10.1038/ncomms5978

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    Other Link： http://www.nature.com/articles/ncomms5978

  • The IRF8-KLF4 transcription factor cascade is essential for the development of monocytes

    Daisuke Kurotaki, Naoki Osato, Akira Nishiyama, Michio Yamamoto, Tatsuma Ban, Hideaki Sato, Jun Nakabayashi, Marina Umehara, Masatoshi Nakazawa, Noriko Miyake, Naomichi Matsumoto, Keiko Ozato, Tomohiko Tamura

    CYTOKINE   63 ( 3 )   279 - 279   2013.9

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    DOI： 10.1016/j.cyto.2013.06.157

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  • Essential role of the IRF8-KLF4 transcription factor cascade in murine monocyte differentiation Reviewed

    Daisuke Kurotaki, Naoki Osato, Akira Nishiyama, Michio Yamamoto, Tatsuma Ban, Hideaki Sato, Jun Nakabayashi, Marina Umehara, Noriko Miyake, Naomichi Matsumoto, Masatoshi Nakazawa, Keiko Ozato, Tomohiko Tamura

    BLOOD   121 ( 10 )   1839 - 1849   2013.3

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    DOI： 10.1182/blood-2012-06-437863

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  • High-mobility group box family of proteins: ligand and sensor for innate immunity Reviewed

    Hideyuki Yanai, Tatsuma Ban, Tadatsugu Taniguchi

    TRENDS IN IMMUNOLOGY   33 ( 12 )   633 - 640   2012.12

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  • Essential role of high-mobility group box proteins in nucleic acid-mediated innate immune responses Invited Reviewed

    Hideyuki Yanai, Tatsuma Ban, Tadatsugu Taniguchi

    JOURNAL OF INTERNAL MEDICINE   270 ( 4 )   301 - 308   2011.10

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    DOI： 10.1111/j.1365-2796.2011.02433.x

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  • A selective contribution of the RIG-I-like receptor pathway to type I interferon responses activated by cytosolic DNA Reviewed

    Myoung Kwon Choi, ZhiChao Wang, Tatsuma Ban, Hideyuki Yanai, Yan Lu, Ryuji Koshiba, Yukana Nakaima, Sho Hangai, David Savitsky, Makoto Nakasato, Hideo Negishi, Osamu Takeuchi, Kenya Honda, Shizuo Akira, Tomohiko Tamura, Tadatsugu Taniguchi

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   106 ( 42 )   17870 - 17875   2009.10

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

    DOI： 10.1073/pnas.0909545106

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  • Regulation of innate immune responses by DAI (DLM-1/ZBP1) and other DNA-sensing molecules Reviewed

    ZhiChao Wang, Myoung Kwon Choi, Tatsuma Ban, Hideyuki Yanai, Hideo Negishi, Yan Lu, Tomohiko Tamura, Akinori Takaoka, Kazuko Nishikura, Tadatsugu Taniguchi

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   105 ( 14 )   5477 - 5482   2008.4

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

    DOI： 10.1073/pnas.0801295105

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MISC

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Presentations

  • 転写因子IRF5に着目した全身性エリテマトーデスの 病態解明と治療法開発 Invited

    藩 龍馬

    第69回日本リウマチ学会総会・学術集会  2025.4 

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    Event date： 2025.4

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  • IRF5 hyperactivation caused by Lyn deficiency is linked to the development of SLE-like disease. International conference

    Tatsuma Ban, Go R. Sato, Akira Nishiyama, Motohide Ichino, Hideyuki Yanai, Akihide Ryo, Tadatsugu Taniguchi, Tomohiko Tamura

    第45回日本免疫学会学術集会  2016.12 

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    Language：English   Presentation type：Oral presentation (general)  

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  • A critical link between Lyn-mediated suppression of the TLR-MyD88-IRF5 pathway and the development of SLE-like disease. International conference

    Tatsuma Ban, Go Sato, Akira Nishiyama, Ai Akiyama, Marie Takasuna, Marina Umehara, Shinsuke Suzuki, Motohide Ichino, Satoko Matsunaga, Ayuko Kimura, Yayoi Kimura, Hideyuki Yanai, Sadakazu Miyashita, Junro Kuromitsu, Kappei Tsukahara, Kentaro Yoshimatsu, Itaru Endo, Tadashi Yamamoto, Hisashi Hirano, Akihide Ryo, Tadatsugu Taniguchi, Tomohiko Tamura

    The Annual Meeting of the American Association of Immunologists 2016  2016.5 

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  • SrcファミリーキナーゼLynによる転写因子IRF5の抑制と全身性エリテマトーデス（SLE）様病態発症との関わり.

    藩龍馬, 佐藤豪, 西山晃, 田村智彦

    第17回神奈川血液・免疫フォーラム  2015.11 

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    Language：Japanese   Presentation type：Oral presentation (general)  

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  • 免疫系転写因子の翻訳後修飾と機能解析を基盤とした自己免疫疾患およびがんの病態解明と治療法開発.

    藩 龍馬, 佐藤 豪, 西山 晃, 松永 智子, 梁 明秀, 木村 鮎子, 木村 弥生, 平野 久, 宮下 定一, 黒光 淳郎, 塚原 克平, 吉松 賢太郎, 田村 智彦

    イノベーションシステム整備事業「翻訳後修飾プロテオミクス医療研究拠点の形成」第6回シンポジウム  2015.10 

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  • IRF5 as a therapeutic target that overcomes the limitation of current therapies in SLE International conference

    Tatsuma Ban, Masako Kikuchi, Go R. Sato, Akio Manabe, Noriko Tagata, Akira Nishiyama, Kenichi Nishimura, Ryusuke Yoshimi, Yohei Kirino, Hideyuki Yanai, Yoshiko Matsumoto, Hiroe Hihara, Masashi Ito, Kappei Tsukahara, Tadashi Yamamoto, Tadatsugu Taniguchi, Hideaki Nakajima, Shuichi Ito, Tomohiko Tamura

    2019 NIH-Japan-JSPS symposium  2019.10 

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  • IRF5 suppression exerts a therapeutic effect beyond type i interferon blockade on murine SLE International conference

    Tatsuma Ban, Masako Kikuchi, Go R. Sato, Akio Manabe, Noriko Tagata, Kenichi Nishimura, Ryusuke Yoshimi, Yohei Kirino, Hideyuki Yanai, Yoshiko Matsumoto, Hiroe Hihara, Masashi Ito, Kappei Tsukahara, Tadatsugu Taniguchi, Hideaki Nakajima, Shuichi Ito, Tomohiko Tamura

    7th Annual Meeting of the International Cytokine & Interferon Society  2019.10 

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  • Selective suppression of IRF5 activity by Lyn in the TLR-MyD88 pathway restrains the development of SLE-like disease. International conference

    Tatsuma Ban, Go Sato, Akira Nishiyama, Satoko Matsunaga, Ayuko Kimura, Yayoi Kimura, Hideyuki Yanai, Yoshiko Matsumoto, Hiroe Hihara, Tadashi Yamamoto, Hisashi Hirano, Akihide Ryo, Kappei Tsukahara, Kentaro Yoshimatsu, Tadatsugu Taniguchi, Tomohiko Tamura

    5th Annual Meeting of the International Cytokine & Interferon Society  2017.10 

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  • LynはTLR-MyD88経路において転写因子IRF5の活性化を抑制することで自己免疫の発症を阻止する.

    藩 龍馬, 佐藤 豪, 田村 智彦

    第13回麒麟塾  2017.7 

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  • Suppression of the TLR-MyD88-IRF5 pathway by the non-receptor type tyrosine kinase Lyn: A critical link to the pathogenesis of SLE. International conference

    Tatsuma Ban, Go R. Sato, Akira Nishiyama, Marie Takasuna, Shinsuke Suzuki, Motohide Ichino, Hideyuki Yanai, Akihide Ryo, Tadatsugu Taniguchi, Tomohiko Tamura

    第43回日本免疫学会学術集会  2014.12 

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  • HMGB proteins function as universal sentinels for nucleic-acid-mediated innate immune responses. International conference

    Tatsuma Ban, Hideyuki Yanai, ZhiChao Wang, Myoung Kwon Choi, Takeshi Kawamura, Hideo Negishi, Makoto Nakasato, Yan Lu, Sho Hangai, Ryuji Koshiba, David Savitsky, Lorenza Ronfani, Shizuo Akira, Marco E. Bianchi, Kenya Honda, Tomohiko Tamura, Tatsuhiko Kodama, Tadatsugu Taniguchi

    第33回日本分子生物学会年会  2010.12 

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  • A selective contribution of the RIG-I-like receptor pathway to type I interferon responses activated by cytosolic DNA. International conference

    Tatsuma Ban, Myoung Kwon Choi, ZhiChao Wang, Hideyuki Yanai, Yan Lu, Ryuji Koshiba, Yukana Nakaima, Sho Hangai, David Savitsky, Makoto Nakasato, Hideo Negishi, Osamu Takeuchi, Kenya Honda, Shizuo Akira, Tomohiko Tamura, Tadatsugu Taniguchi

    第32回日本分子生物学会年会  2009.12 

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  • 転写因子IRF5の遺伝学的手法および化合物による阻害はマウスSLEモデルにおいて治療効果を示す

    藩 龍馬, 菊地 雅子, 佐藤 豪, 田村 智彦

    第17回麒麟塾  2022.7 

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  • Therapeutic effects of genetic and chemical targeting of IRF5 on experimental SLE

    Ban T, Kikuchi M, Sato GR, Manabe A, Nishiyama A, Yoshimi R, Yanai H, Yamamoto T, Taniguchi T, Ito S, Tamura T

    2021.12 

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  • 全身性エリテマトーデスにおける転写因子IRF5の阻害は現行治療法の限界を克服した新規治療法となる可能性がある

    藩 龍馬, 佐藤 豪, 菊地 雅子, 西村 謙一, 吉見 竜介, 桐野 洋平, 松本 佳子, 日原 裕恵, 伊藤 昌史, 塚原 克平, 中島 秀明, 伊藤 秀一, 田村 智彦

    第85回日本インターフェロン・サイトカイン学会学術集会  2021.5 

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Industrial property rights

  • 免疫チェックポイント阻害剤治療の治療選択を補助する指標の評価方法、算出方法、評価装置、算出装置、評価プログラム、算出プログラム、評価システム、及び端末装置

    笹田哲朗, 東公一, 室谷健太, 田上智行, 萩原麻美, 今泉明, 唐川幸聖, 川崎美佳, 宮城洋平, 田村智彦, 齋藤春洋, 中原善朗, 魏菲菲, 笠島理加, 項慧慧, 藩龍馬

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    Applicant：地方独立行政法人神奈川県立病院機構;味の素株式会社

    Application no：PCT/JP2023/013821  Date applied：2023.4

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  • 活性型IRF5を特異的に認識するモノクローナル抗体

    田村智彦, 藩龍馬

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    Application no：特願2019-107741  Date applied：2019.6

    Patent/Registration no：特許第7311883号  Date registered：2023.7 

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Awards

  • Milstein Travel Award

    2019.10   International Cytokine & Interferon Society  

    藩 龍馬

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  • Milstein Young Investigator Award

    2017.10   International Cytokine & Interferon Society  

    BAN Tatsuma

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  • Research Award

    2017.5   Yokohama City University Medical Association  

    BAN Tatsuma

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Research Projects

  • 転写因子IRF5を介した自己免疫関連B細胞の生成メカニズムの解明

    Grant number：25K10402  2025.4 - 2028.3

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    藩 龍馬

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    Grant amount：\4550000 （ Direct Cost: \3500000 、 Indirect Cost：\1050000 ）

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  • p53異常子宮体癌におけるTAM関連分子の抗腫瘍免疫応答に対する作用の解明

    2025.1 - 2026.3

    神澤医学研究振興財団  2024年度 研究助成金 

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    Authorship：Principal investigator 

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  • 腫瘍関連マクロファージ関連遺伝子に注目した2型子宮体癌の創薬ターゲットの確立

    2024.8 - 2029.3

    武⽥科学振興財団  2024年度 研究助成 

    藩 龍馬

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  • 心筋炎から心筋症への移行を阻止する全く新しい特発性拡張型心筋症の治療法開発に向けた病態解明と治療標的同定

    2023.9 - 2026.3

    日本医療研究開発機構  難治性疾患実用化研究事業 

    藩 龍馬

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    Authorship：Principal investigator 

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  • 新規自己炎症性疾患 VEXAS症候群のdeep phenotypingを通じた病態解明研究

    2023.4 - 2026.3

    日本医療研究開発機構  免疫アレルギー疾患実用化研究事業 

    桐野 洋平

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    Authorship：Coinvestigator(s) 

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  • 転写因子IRF5に注目した全身性エリテマトーデスの新しい病態解明

    2023.4 - 2026.3

    日本医療研究開発機構  難治性疾患実用化研究事業 

    田村 智彦

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    Authorship：Coinvestigator(s) 

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  • 転写因子IRF5阻害剤による全身性エリテマトーデスの革新的治療法とそのコンパニオン診断法の開発

    2020.11 - 2023.3

    日本医療研究開発機構  免疫アレルギー疾患等実用化研究事業 

    田村 智彦

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  • 自己免疫疾患における形質細胞様樹状細胞の機能疲弊についての解析

    2019.7 - 2021.7

    横浜総合医学振興財団  令和元年度 推進研究助成 

    藩 龍馬

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    Authorship：Principal investigator  Grant type：Competitive

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  • 樹状細胞における転写因子IRF5の新規機能解明

    2018.4 - 2019.3

    上原記念生命科学財団  平成29年度 研究奨励金 

    藩 龍馬

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    Authorship：Principal investigator  Grant type：Competitive

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  • 全身性エリテマトーデスの革新的治療法のための転写因子IRF5阻害剤の開発

    2017.4 - 2020.3

    日本医療研究開発機構  免疫アレルギー疾患等実用化研究事業 

    田村 智彦

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    Authorship：Coinvestigator(s)  Grant type：Competitive

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  • SLEの治療法開発に向けたIRF5選択的制御メカニズムの解明

    2016.4 - 2019.3

    日本学術振興会  平成28年度 若手研究(B) 

    藩 龍馬

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    Authorship：Principal investigator  Grant type：Competitive

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  • 自然免疫応答における新規転写因子制御機構の解明

    2013.4 - 2016.3

    日本学術振興会  平成25年度 若手研究（Ｂ） 

    藩 龍馬

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    Authorship：Principal investigator  Grant type：Competitive

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  • 自然免疫系におけるDNA認識受容体の解析

    Grant number：09J05310  2009 - 2011

    日本学術振興会  科学研究費助成事業 特別研究員奨励費  特別研究員奨励費

    藩 龍馬

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    Grant amount：\2100000 （ Direct Cost: \2100000 ）

    核酸を介した免疫応答は、細菌やウイルスなどの病原体に対する生体防御に重要である一方、自己免疫疾患や炎症などの病態とも密接な関係が指摘されている。前年度までの研究において、High mobility group box(HMGB)と呼ばれる分子群(HMGB1～3)が核酸による免疫応答に重要であり、病原体由来の核酸を汎く認識できる万能な核酸センサーであることを見出し、論文としてNature誌に発表した。
    当該年度においては、上記で得られた知見を基に、HMGBと強く結合し、免疫原性を持たないオリゴDNA(oligodeoxynucleotides ; ODN)を作製し、それらがHMGBの機能を阻害することにより、核酸を介した免疫応答の活性化に与える影響を検討した。その結果、作製した非免疫原性ODNが、核酸による自然免疫応答を強く抑制することを見出した。さらに、自己免疫疾患である多発性硬化症のマウスモデルである実験的自己免疫性脳脊髄炎(Experimental autoimmune encephalomyelitis ; EAE)やHMGBが関与していることが知られている敗血症性ショックモデルにおいて、この非免疫原性ODNを投与することにより病態が顕著に軽減されることが示された。
    これらの結果は、自然免疫系における核酸認識機構の解明に新たな知見を供するものであり、自己免疫疾患などの治療応用に適用できる可能性があると考えられる。また、これらの研究結果は論文としてProc. Natl. Acad. Sci. USA誌に発表した。

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