Kiura Kazuto, Kataoka Hideo, Nakata Takashi, Into Takeshi, Yasuda Motoaki, Akira Shizuo, Inoue Nobuo, Shibata Ken-ichiro
Department of Oral Pathobiological Science, Hokkaido University Graduate School of Dental Medicine, Nidhi 7, Kita 13, Kita-ku, Sapporo 060-8586, Japan.
FEMS Immunol Med Microbiol. 2006 Feb;46(1):78-84. doi: 10.1111/j.1574-695X.2005.00002.x.
Granulocyte-macrophage colony-stimulating factor-differentiated bone marrow-derived dendritic cells were stimulated with the synthetic lipopeptide S-(2,3-bispalmitoyloxypropyl)-CGDPKHSPKSF (FSL-1) or the Escherichia coli lipopolysaccharide. FSL-1 induced the production of TNF-alpha and IL-12 by C57BL/6-derived bone marrow-derived dendritic cells but not by bone marrow-derived dendritic cells from Toll-like receptor 2-deficient (TLR2(-/-)) mice. Lipopolysaccharide induced the production of TNF-alpha and IL-12 by bone marrow-derived dendritic cells derived from either type of mice. FSL-1 did not induce production of IL-10 by bone marrow-derived dendritic cells from either type of mice, whereas lipopolysaccharide induced small amounts of IL-10 by bone marrow-derived dendritic cells from both types of mice. The upregulation by FSL-1 of the expression of CD80, CD86 and the MHC class II molecule IA(b) was dose- and time-dependent on the surfaces of C57BL/6-derived bone marrow-derived dendritic cells but not on the surface of TLR2(-/-)-derived bone marrow-derived dendritic cells. Lipopolysaccharide upregulated the expression of these molecules on the surfaces of bone marrow-derived dendritic cells from both types of mice. The expression of CD11c on the surfaces of C57BL/6-derived bone marrow-derived dendritic cells was upregulated by stimulation with both FSL-1 and lipopolysaccharide up to 12 h; thereafter, the expression was downregulated. The results suggest that FSL-1 can accelerate maturation of bone marrow-derived dendritic cells and this FSL-1 activity is mediated by TLR2.
用合成脂肽S-(2,3-双棕榈酰氧基丙基)-CGDPKHSPKSF（FSL-1）或大肠杆菌脂多糖刺激粒细胞-巨噬细胞集落刺激因子分化的骨髓来源树突状细胞。FSL-1可诱导C57BL/6来源的骨髓来源树突状细胞产生肿瘤坏死因子-α（TNF-α）和白细胞介素-12（IL-12），但不能诱导Toll样受体2缺陷（TLR2(-/-)）小鼠的骨髓来源树突状细胞产生。脂多糖可诱导两种小鼠来源的骨髓来源树突状细胞产生TNF-α和IL-12。FSL-1不能诱导两种小鼠来源的骨髓来源树突状细胞产生IL-10，而脂多糖可诱导两种小鼠来源的骨髓来源树突状细胞产生少量IL-10。FSL-1对C57BL/6来源的骨髓来源树突状细胞表面CD80、CD86和MHC II类分子IA(b)表达的上调呈剂量和时间依赖性，但对TLR2(-/-)来源的骨髓来源树突状细胞表面无此作用。脂多糖上调了两种小鼠来源的骨髓来源树突状细胞表面这些分子的表达。FSL-1和脂多糖刺激均可使C57BL/6来源的骨髓来源树突状细胞表面CD11c的表达上调至12小时；此后，表达下调。结果表明，FSL-1可加速骨髓来源树突状细胞的成熟，且这种FSL-1活性由TLR2介导。
