クリプトシアニン色素（NK-4）によるNatural Killer T （NKT）細胞活性化作用

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  • 國方 敏夫
    株式会社林原生物化学研究所研究センター医薬研究部門
  • 河野 恵三
    株式会社林原生物化学研究所研究センター医薬研究部門
  • 牛尾 慎平
    株式会社林原生物化学研究所研究センター医薬研究部門
  • 福田 恵温
    株式会社林原生物化学研究所研究センター医薬研究部門

書誌事項

タイトル別名
  • Activation of Natural Killer T Cells by NK-4, a Criptocyanine Dye
  • クリプトシアニン シキソ(NK-4)ニ ヨル Natural Killer T (NKT)サイボウ カッセイカ サヨウ

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説明

We previously reported that oral administration of NK-4, a criptocyanine dye, enhances interleukin (IL)-12-depend- ent interferon (IFN)-γ production by lipopolysaccharide (LPS)-stimulated mouse splenocytes. These findings raised a possibility that NK-4 potentiated IFN-γ production by T cells, natural killer (NK) cells or natural killer T (NKT) cells in response to IL-12 produced by macrophage and dendritic cells. To explore this possibility, we first analyzed percentages of T, NK or NKT cells in splenocytes of mice that were administered NK-4 orally for three days. The percentage of NKT cells in splenocytes from NK-4-treated mice was significantly (p<0.05) increased compared to vehicle-treated mice. When splenocytes were stimulated with α-galactosylceramide (α-GalCer), an NKT cell ligand, IFN-γ production by splenocytes from NK-4-treated mice tended to increase, while no difference in the IL-4 production and proliferation were observed between the vehicle- and NK-4-treated mice. When IFN-γ/IL-4 ratios were calculated in individual mice, the ratios were significantly (p<0.05) elevated in NK-4-treated mice. Furthermore, IL-12 production by α-GalCer-stimulated splenocytes from NK-4-treated mice was also significantly (p<0.05) increased. These results suggest that oral administration of NK-4 increases the population of type I NKT cells with potent IFN-γ-producing activities. Since IL-12 and IFN-γ have been shown to play important roles in anti-tumor immunity as well as in the defence against bacterial infection, our results further imply that NK-4 may provide a potential therapeutic tool in cancer immunotherapy.<br>

収録刊行物

  • 薬学雑誌

    薬学雑誌 131 (11), 1667-1674, 2011-11-01

    公益社団法人 日本薬学会

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