東北大学大学院医学系研究科・医学部

STAFF

Professor

• Hiroshi, FujiiProfessor. 藤井 博司 教授
  

Other Faculty / Staff

• Gohno, Tatsuyuki

  Assistant Prof. 郷野 辰幸 助教

CONTACT

OUTLINE

The department of Clinical Immunology and Rheumatology was established in April 2024. Our laboratory, closely affiliated with the division of Rheumatology at Tohoku University Hospital, conducts research on collagen diseases. We focus particularly on systemic lupus erythematosus and vasculitic syndromes, investigating the mechanisms of autoantibody production, the processes of lesion formation, and the development of novel therapies for these diseases. Our research primarily utilizes serum and cells obtained from patients with collagen diseases to elucidate the pathogenesis. Notably, our original method of identifying cell surface autoantigens, SARF (serological identification system for autoantibodies using a retroviral vector and flow cytometry), has identified autoantigens that propose new pathological mechanisms in Takayasu arteritis, drawing significant attention. We also conduct research using animal models to deepen our understanding of disease mechanisms and evaluate insights obtained from human diseases. We are seeking passionate young researchers who are driven to uncover the mysteries of autoimmune diseases. If you are interested in conducting research that fundamentally elucidates diseases and develops novel treatments to transform clinical practice, please contact our laboratory.

臨床免疫学分野は2024年4月に設立されました。私たちの研究室は、東北大学病院リウマチ膠原病内科と密接な関係をもち、膠原病の研究を行っています。特に全身性エリテマトーデスや血管炎症候群に注目し、これらの疾患で認められる自己抗体の産生機序や病変形成の過程、その制御法の開発について追求しています。 研究手法としては、実際の膠原病患者から得た血清や細胞を用いた実験を主軸に置き、病態の解明を行っています。なかでも独自に開発した細胞表面の自己抗原同定法、SARF（serological identification system for autoantibodies using a retroviral vector and flowcytometry）により同定された自己抗原は、高安動脈炎における新しい病態を提唱し、注目されています。ヒト疾患から得られた知見の評価と疾患の機序の理解を深めるために、動物モデルを用いた研究も行っています。 私たちは、自己免疫疾患の本質に迫ることに情熱を持つ若い研究者を求めています。病気の根本的な解明を通じて、より良い治療法の開発、臨床の現場を変える研究をしてみたいと考えている方は、ぜひ当研究室にご連絡ください。

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  Mechanism of inflammarion by autoantibodies in Takayasu arteritis
  高安動脈炎における自己抗体

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  Laboratory and equipment
  実験室と実験機器

ARTICLE

Yasaka K, et al. Phospholipase D4 as a signature of toll-like receptor 7 or 9 signaling is expressed on blastic T-bet + B cells in systemic lupus erythematosus. Arthritis Res Ther. 25 (1):200, 2023
URL：https://arthritis-research.biomedcentral.com/articles/10.1186/s13075-023-03186-5

Akita K, et al. Interferon α enhances B cell activation associated with FOXM1 induction: potential novel therapeutic strategy for targeting the plasmablasts of systemic lupus erythematosus. Front Immunol 11:498703, 2021
URL：https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2020.498703/full

Mutoh T, et al. Identification of two major autoantigens negatively regulating endothelial activation in Takayasu arteritis. Nat Commun. 11(1):1253, 2020
URL：https://www.nature.com/articles/s41467-020-15088-0

Ikeda T, et al. Bortezomib treatment induces a higher mortality rate in lupus model mice with a higher disease activity. Arthritis Res Ther. 19(1):187, 2017
URL：https://arthritis-research.biomedcentral.com/articles/10.1186/s13075-017-1397-7

Shirai T, et al. An innovative method to identify autoantigens expressed on the endothelial cell surface: serological identification system for autoantigens using a retroviral vector and flow cytometry (SARF) Clin Dev Immunol. 2013:453058, 2013
URL：https://www.hindawi.com/journals/jir/2013/453058/