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Development of a novel therapy using anti-CX3CL1 antibody in systemic sclerosis

Research Project

Project/Area Number 15K09763
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Dermatology
Research InstitutionUniversity of Fukui

Principal Investigator

Hasegawa Minoru  福井大学, 学術研究院医学系部門, 教授 (50283130)

Project Period (FY) 2015-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Keywords強皮症 / CX3CL1 / 新規治療 / 疾患モデル / 線維化 / 血管障害 / 治療 / ケモカイン / マクロファージ
Outline of Final Research Achievements

We investigated the efficacy of anti-mouse CX3CL1 monoclonal antibody (mAb) therapy for skin lesion in two different mouse models of systemic sclerosis (SSc). In the first model, daily subcutaneous bleomycin injections induced skin fibrosis and vascular injury subsequent to inflammation in C57BL/6 mice. However, administration of anti-CX3CL1 mAb or CX3CR1 deficiency significantly inhibited them via reduced dermal infiltration of CX3CR1+ cells. Results of RNA sequencing and qRT-PCR demonstrated that expression of fibrogenic molecules induced by bleomycin injection, was significantly suppressed by anti-CX3CL1 mAb therapy. In the second model, BALB/c newborn mice received subcutaneous injections of TGF-β followed by that of CTGF. However, pretreatment of anti-CX3CL1 mAb significantly inhibited the skin fibrosis and inflammation of this model. No obvious side effects were found. Anti-CX3CL1 mAb therapy could be a novel approach for inflammatory-driven fibrotic skin disorders.

Report

(4 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report
  • 2015 Research-status Report
  • Research Products

    (4 results)

All 2018 2017 2016 2015

All Presentation (4 results) (of which Int'l Joint Research: 1 results)

  • [Presentation] Blockade of CX3CL1-CX3CR1 pathway attenuates skin inflammation, fibrosis, and vascular injury in experimental mouse models of systemic sclerosis2018

    • Author(s)
      Vu Huy Luong, Takenao Chino, Noritaka Oyama, Takashi Matsushita, Takashi Obara, Yoshikazu Kuboi, Naoto Ishii, Akihito Machinaga, Hideaki Ogasawara, Wataru Ikeda, Toshio Imai, Minoru Hasegawa
    • Organizer
      International Investigative Dermatology 2018
    • Related Report
      2017 Annual Research Report
    • Int'l Joint Research
  • [Presentation] Anti-CX3CL1 antibody therapy attenuates the development of inflammation, fibrosis, and vascular injury2017

    • Author(s)
      Vu H. Luong, Takenao Chino, Noritaka Oyama, Takashi Obara, Yoshikazu Kuboi, Naoto Ishii, Akihito Machinaga, Hideaki Ogasawara, Wataru Ikeda, Toshio Imai, Minoru Hasegawa
    • Organizer
      日本研究皮膚科学会第42回年次学術大会・総会
    • Related Report
      2017 Annual Research Report
  • [Presentation] Anti-CX3CL1 antiboby therapy attenuates the development of bleomycin-induced and growth factors-induced skin fibrosis in mice.2016

    • Author(s)
      Vu H.Luong, Chino T, Oyama N, Kuboi Y, Obara T, Machinaga A, Ogasawara H, Ikeda W, Imai T, Hasegawa M.
    • Organizer
      第45回日本免疫学会総会・学術集会
    • Place of Presentation
      沖縄コンベンションセンター、ラグナガーデンホテル(沖縄県那覇市)
    • Year and Date
      2016-12-05
    • Related Report
      2016 Research-status Report
  • [Presentation] Anti-CX3CL1 monoclonal antiboby: a promising therapy for systemic sclerosis.2015

    • Author(s)
      Vu H.Luong, Chino T, Tokuriki A, Oyama N, Hasegawa M, Kuboi Y, Obara T, Yasuda N, Muramoto K, Imai T.
    • Organizer
      日本研究皮膚科学会第40回年次学術大会・総会
    • Place of Presentation
      岡山市
    • Year and Date
      2015-12-11
    • Related Report
      2015 Research-status Report

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Published: 2015-04-16   Modified: 2019-03-29  

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