竹下　勝 （タケシタ　マサル）

Takeshita, Masaru

写真a

所属（所属キャンパス）

医学部 内科学教室（リウマチ・膠原病） （信濃町）

職名

専任講師（有期）
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研究分野 【 表示 ／ 非表示 】

  • 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 / 膠原病、アレルギー内科学

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研究テーマ 【 表示 ／ 非表示 】

  • 膠原病の病変組織に浸潤したリンパ球の解析, 

    2015年04月
    -
    継続中

  • 滑膜モデルの作成, 

    2015年04月
    -
    継続中

  • helper T細胞の分化, 

    2014年04月
    -
    継続中

  • 膠原病の糖タンパクバイオマーカー探索, 

    2013年04月
    -
    継続中

  • 各種膠原病のHLAとの関連に関する研究, 

    2013年04月
    -
    継続中

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論文 【 表示 ／ 非表示 】

  • Significant association between joint ultrasonographic parameters and synovial inflammatory factors in rheumatoid arthritis

    Kondo Y., Suzuki K., Inoue Y., Sakata K., Takahashi C., Takeshita M., Kassai Y., Miyazaki T., Morita R., Niki Y., Kaneko Y., Yasuoka H., Yamaoka K., Yoshimura A., Takeuchi T.

    Arthritis Research and Therapy （Arthritis Research and Therapy）  21 （ 1 ）  2019年10月

    ISSN  14786354

    　概要を見る

    © 2019 The Author(s). Background: Ultrasonography (US) can directly demonstrate joint inflammation, including grayscale (GS) signs of synovial hypertrophy and power Doppler (PD) techniques to demonstrate increased blood flow and vascularization. Recently, echogenicity, especially hypoechoic synovium, has also been associated with local inflammatory activity. However, only a few studies have demonstrated correlation between histopathologic and immunopathologic evaluation and US findings. The aim of this study was to clarify whether joint US findings including synovial hypertrophy, vascularity, and echogenicity can accurately characterize synovial pathophysiology in patients with active rheumatoid arthritis (RA). Methods: A total of 44 patients with RA were included, both treated (n = 25) and untreated (n = 19) and scheduled for US examination of the knee joint with synovial fluid (SF) aspiration and two treated patients also underwent synovial biopsy. US images were quantitatively analyzed using grayscale assessment of synovial hypertrophy and PD for vascularity and echogenicity. Levels of nine SF cytokines and growth factors were also measured. Results: Both US synovial hypertrophy and PD vascularity significantly correlated with SF inflammatory cytokine levels such as IL-6, IL-8, IL-1β and IL-10 in untreated patients. Angiogenic factors, including vascular endothelial growth factor (VEGF), only correlated with PD vascularity. In the treated patients, the associations between synovial hypertrophy and any cytokines were diminished, although synovial vascularity and echogenicity correlated with IL-6 and VEGF (p < 0.05). Histopathologic analysis revealed that hypoechogenicity of the synovium correlated with marked infiltration of lymphocytes and hypervascularity. Conclusions: We demonstrated the pathophysiological origins of US findings in the joint. The degree of US vascularity of the synovium correlated with local inflammatory cytokine levels and angiogenetic factors in patients with active RA. Synovial echogenicity, and not hypertrophy, correlated with inflammation, especially in treated patients with RA.

  • Multi-omics monitoring of drug response in rheumatoid arthritis in pursuit of molecular remission

    Tasaki S., Suzuki K., Kassai Y., Takeshita M., Murota A., Kondo Y., Ando T., Nakayama Y., Okuzono Y., Takiguchi M., Kurisu R., Miyazaki T., Yoshimoto K., Yasuoka H., Yamaoka K., Morita R., Yoshimura A., Toyoshiba H., Takeuchi T.

    Nature Communications （Nature Communications）  9 （ 1 ）  2018年12月

    　概要を見る

    © 2018 The Author(s). Sustained clinical remission (CR) without drug treatment has not been achieved in patients with rheumatoid arthritis (RA). This implies a substantial difference between CR and the healthy state, but it has yet to be quantified. We report a longitudinal monitoring of the drug response at multi-omics levels in the peripheral blood of patients with RA. Our data reveal that drug treatments alter the molecular profile closer to that of HCs at the transcriptome, serum proteome, and immunophenotype level. Patient follow-up suggests that the molecular profile after drug treatments is associated with long-term stable CR. In addition, we identify molecular signatures that are resistant to drug treatments. These signatures are associated with RA independently of known disease severity indexes and are largely explained by the imbalance of neutrophils, monocytes, and lymphocytes. This high-dimensional phenotyping provides a quantitative measure of molecular remission and illustrates a multi-omics approach to understanding drug response.

  • Alteration of matrix metalloproteinase-3 O-glycan structure as a biomarker for disease activity of rheumatoid arthritis

    竹下 勝, 他　

    Arthritis Research & Therapy 18 （ 112 ）  2016年05月

    研究論文（学術雑誌）, 共著, 査読有り

  • Polarization diversity of human CD4(+) stem cell memory T cells

    竹下 勝

    CLINICAL IMMUNOLOGY 159 （ 1 ） 107 - 117 2015年07月

    研究論文（学術雑誌）,  ISSN  1521-6616

  • Distinct Serum Protein Signature and Novel Biomarkers of primary Sjogren's Syndrome Revealed by comprehensive High-Throughput Proteomic Analysis.

    竹下 勝

    ARTHRITIS &amp; RHEUMATOLOGY 66   S1301 - S1302 2014年10月

    研究論文（学術雑誌）,  ISSN  2326-5191

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競争的研究費の研究課題 【 表示 ／ 非表示 】

  • 自己免疫疾患の病変部位における自己抗体の産生機構の解明

    2022年04月
    -
    2025年03月

    文部科学省・日本学術振興会, 科学研究費助成事業, 竹下 勝, 基盤研究(C), 補助金,  研究代表者

  • 自己免疫疾患の根治を目標とする抗原特異性と遺伝子発現のシングルセル統合解析

    2020年04月
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    2022年03月

    文部科学省・日本学術振興会, 科学研究費助成事業, 竹下 勝, 若手研究, 補助金,  研究代表者

  • 自己免疫疾患における新しい抗原提示機構とその意義について

    2016年04月
    -
    2019年03月

    文部科学省・日本学術振興会, 科学研究費助成事業, 竹下　勝, 若手研究(B), 補助金,  研究代表者

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