title: [Activation of natural killer T cells by NK-4, a criptocyanine dye].
abstract: 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.
authors: Biomedical Institute, Research Center, Hayashibara Biochemical Laboratories, Inc., Okayama, Japan. t-kuni@hayashibara.co.jp
authors: Toshio
authors: T
authors: Kunikata
authors: Keizo
authors: K
authors: Kohno
authors: Shimpei
authors: S
authors: Ushio
authors: Shigeharu
authors: S
authors: Fukuda
mesh_terms: D060433:Administration, Ophthalmic; D000818:Animals; D000970:Antineoplastic Agents; D002478:Cells, Cultured; D004396:Coloring Agents / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D005699:Galactosylceramides / Q000494:pharmacology; D007371:Interferon-gamma / Q000096:biosynthesis; D018664:Interleukin-12 / Q000096:biosynthesis; D008024:Ligands; D008213:Lymphocyte Activation / Q000187:drug effects*; D051379:Mice; D008810:Mice, Inbred C57BL; D055611:Natural Killer T-Cells / Q000276:immunology*; D011806:Quinolinium Compounds / Q000008:administration & dosage / Q000494:pharmacology*; D013154:Spleen / Q000166:cytology; D013268:Stimulation, Chemical
chemical_list: D000970:Antineoplastic Agents; D004396:Coloring Agents; D005699:Galactosylceramides; D008024:Ligands; D011806:Quinolinium Compounds; C493154:alpha-galactosylceramide; D018664:Interleukin-12; D007371:Interferon-gamma