論文

国際誌
2019年11月

Targeting inflammatory sites through collagen affinity enhances the therapeutic efficacy of anti-inflammatory antibodies.

Science advances
  • Kiyomitsu Katsumata
  • ,
  • Jun Ishihara
  • ,
  • Aslan Mansurov
  • ,
  • Ako Ishihara
  • ,
  • Michal M Raczy
  • ,
  • Eiji Yuba
  • ,
  • Jeffrey A Hubbell

5
11
開始ページ
eaay1971
終了ページ
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1126/sciadv.aay1971

Enhancing the therapeutic efficacy of drugs for inflammatory diseases is of high demand. One possible approach is targeting drugs to the extracellular matrix of the inflamed area. Here, we target collagens in the matrix, which are inaccessible in most tissues yet are exposed to the bloodstream in the inflamed area because of vascular hyperpermeability. We conferred collagen affinity to anti-tumor necrosis factor-α (α-TNF) antibody by conjugating a collagen-binding peptide (CBP) derived from the sequence of decorin. CBP-α-TNF accumulated in the inflamed paw of the arthritis model, and arthritis development was significantly suppressed by treatment with CBP-α-TNF compared with the unmodified antibody. Similarly, CBP-anti-transforming growth factor-β (α-TGF-β) accumulated in the inflamed lung of pulmonary fibrosis model and significantly suppressed pulmonary fibrosis compared with the unmodified antibody. Together, collagen affinity enables the anticytokine antibodies to target arthritis and pulmonary fibrosis accompanied by inflammation, demonstrating a clinically translational approach to treat inflammatory diseases.

リンク情報
DOI
https://doi.org/10.1126/sciadv.aay1971
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/31723606
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834392
ID情報
  • DOI : 10.1126/sciadv.aay1971
  • PubMed ID : 31723606
  • PubMed Central 記事ID : PMC6834392

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