Toll样受体和髓样分化因子88基因敲除小鼠的树突状细胞功能
Dendritic-cell function in Toll-like receptor- and MyD88-knockout mice.
作者信息
Kaisho T, Akira S
机构信息
Dept of Host Defense, Research Institute for Microbial Diseases, Osaka University, Yamadaoka 3-1, Suita, 565-0871, Osaka, Japan.
出版信息
Trends Immunol. 2001 Feb;22(2):78-83. doi: 10.1016/s1471-4906(00)01811-1.
Based on recent findings in myeloid differentiation factor 88 (MyD88)- and Toll-like receptor (TLR)-knockout mice, Tsuneyasu Kaisho and Shizuo Akira discuss the roles of TLRs and MyD88 in dendritic cell (DC) maturation and cytokine production. Lipopolysaccharide binds TLR4 and can induce DC maturation in the absence of MyD88, whereas CpG DNA binds TLR9 and induces DC maturation in a MyD88-dependent manner.
基于近期在髓样分化因子88（MyD88）和Toll样受体（TLR）基因敲除小鼠中的研究发现，海绍恒安和赤木史郎讨论了TLR和MyD88在树突状细胞（DC）成熟及细胞因子产生中的作用。脂多糖结合TLR4，且在没有MyD88的情况下可诱导DC成熟，而CpG DNA结合TLR9并以MyD88依赖的方式诱导DC成熟。
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