英语翻译endritic cells have been described.Murine dendritic cell
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英语翻译
endritic cells have been described.Murine dendritic cells express the CD11c integrin and can be subdivided on the basis of CD8a expression.A third population of murine +CD11c cells,also expressing B220 and Gr-1,is equiva lent to human plasmacytoid dendritic cells (Colonna et al.
2002).Notably,recent evidence suggests that CD8a is a marker for the maturation stage of dendritic cells rather than different lineages (Martinez del Hoyo et al.,2002) Dendritic cell subtypes may differ in their expression oTLRs.In humans,only plasmacytoid dendritic cells,but
not myeloid dendritic cells,express TLR9,the receptor for unmethylated CpG motifs that are abundant in bacterial DNA.Genetically determined differences in the composition of dendritic cell subsets may therefore be associated with resistance and susceptibility to infection with a given pathogen.In concordance with this suggestion,it has been shown that dendritic cells from mice that are resistant to infection with Listeria monocytogenes preferentially express TLR9,together with the dendritic cell maturation markers CD40 and CD86,and produce high levels of IL-12,whereas dendritic cells from susceptible mice strongly express TLR2,-4,-5,and -6,and produce larger amounts of MCP-1 (Liu et al.,2002).The intracellular signalling pathways activated by TLRs involve recruitment of the cytoplasmic adaptor molecule MyD88,activation of serine/threonine kinases of the IRAK family,and finally degradation of IkB and translocation of NF-kB to the nucleus (Akira et al.,2001).Recently,a MyD88-independent pathway has been shown to be responsible for the induction of IFN-b and IFN-inducible genes (Akira,2003).In mice lacking MyD88,host resistance to infection with the intracellular protozoan Toxoplasma gondii and parasite-induced IL-12 production by dendritic cells was shown to be dramatically reduced (Scanga et al.,
2002).Because dendritic cells from mice de?cient in TLR2 or TLR4 mounted normal IL-12 responses to T.gondii antigen,these TLRs do not seem to be involved in the IL-12 response to this parasite.In contrast,TLR2 triggering has been demonstrated to play a role in the induction of
cytokines by glycolipid antigens of Trypanosoma cruzi (Campos et al.,2001) and by purified protein derivative of Mycobacterium tuberculosis
endritic cells have been described.Murine dendritic cells express the CD11c integrin and can be subdivided on the basis of CD8a expression.A third population of murine +CD11c cells,also expressing B220 and Gr-1,is equiva lent to human plasmacytoid dendritic cells (Colonna et al.
2002).Notably,recent evidence suggests that CD8a is a marker for the maturation stage of dendritic cells rather than different lineages (Martinez del Hoyo et al.,2002) Dendritic cell subtypes may differ in their expression oTLRs.In humans,only plasmacytoid dendritic cells,but
not myeloid dendritic cells,express TLR9,the receptor for unmethylated CpG motifs that are abundant in bacterial DNA.Genetically determined differences in the composition of dendritic cell subsets may therefore be associated with resistance and susceptibility to infection with a given pathogen.In concordance with this suggestion,it has been shown that dendritic cells from mice that are resistant to infection with Listeria monocytogenes preferentially express TLR9,together with the dendritic cell maturation markers CD40 and CD86,and produce high levels of IL-12,whereas dendritic cells from susceptible mice strongly express TLR2,-4,-5,and -6,and produce larger amounts of MCP-1 (Liu et al.,2002).The intracellular signalling pathways activated by TLRs involve recruitment of the cytoplasmic adaptor molecule MyD88,activation of serine/threonine kinases of the IRAK family,and finally degradation of IkB and translocation of NF-kB to the nucleus (Akira et al.,2001).Recently,a MyD88-independent pathway has been shown to be responsible for the induction of IFN-b and IFN-inducible genes (Akira,2003).In mice lacking MyD88,host resistance to infection with the intracellular protozoan Toxoplasma gondii and parasite-induced IL-12 production by dendritic cells was shown to be dramatically reduced (Scanga et al.,
2002).Because dendritic cells from mice de?cient in TLR2 or TLR4 mounted normal IL-12 responses to T.gondii antigen,these TLRs do not seem to be involved in the IL-12 response to this parasite.In contrast,TLR2 triggering has been demonstrated to play a role in the induction of
cytokines by glycolipid antigens of Trypanosoma cruzi (Campos et al.,2001) and by purified protein derivative of Mycobacterium tuberculosis
endritic细胞被描述.小鼠树突状细胞表达CD11c整合和可细分的基础上, CD8a表达.第三次人口小鼠+ CD11c细胞,还表达B220和GR - 1 ,是等价借给人类浆树突状细胞(科隆纳等.
2002年) .值得注意的是,最近的迹象表明, CD8a是一个成熟的标志阶段的树突状细胞,而不是不同的谱系(马丁尼兹格雷贝尔德尔奥约等人. , 2002年)树突状细胞亚型可能会有不同的表达oTLRs .在人类中,只有浆树突状细胞,但
髓系树突状细胞不表达TLR9 ,该受体的甲基CpG基序中有丰富的细菌DNA .基因差异决定组成树突状细胞亚群,可能有相关性和敏感性,以感染特定病原体.和谐这一建议,它已经表明,从小鼠树突状细胞的抗感染李斯特菌优先表达TLR9 ,连同树突状细胞的成熟标志CD40分子和CD86 ,并产生高水平的IL - 12的,而树突状细胞从易感小鼠强烈表示TLR2 , -4 , -5和-6 ,并产生大量的趋化蛋白-1 (刘等人. , 2002年) .细胞内信号途径激活受体参与招聘细胞质接头分子MyD88 ,激活的丝氨酸/苏氨酸激酶的义IRAK家庭,并最终降解IkB和易位的NF - kB的核(彰等人. , 2001年) .最近, MyD88依赖性途径已被证明是负责的诱导干扰素- B和干扰素诱导基因(明, 2003年) .在小鼠体内缺乏MyD88 ,东道国抗感染细胞原生动物弓形虫和寄生虫引起的IL - 12的生产树突状细胞被证明是大大减少( Scanga等. ,
2002年) .由于树突状细胞的小鼠日?系数在TLR2或Toll样受体4安装正常IL - 12的答复弓形虫抗原,这些受体似乎并不参与IL - 12的回应这种寄生虫.与此相反, TLR2触发已经证明中发挥作用的诱导
细胞因子的糖脂抗原的克氏锥虫(坎波斯等. , 2001年)和纯蛋白衍生物的结核分枝杆菌
2002年) .值得注意的是,最近的迹象表明, CD8a是一个成熟的标志阶段的树突状细胞,而不是不同的谱系(马丁尼兹格雷贝尔德尔奥约等人. , 2002年)树突状细胞亚型可能会有不同的表达oTLRs .在人类中,只有浆树突状细胞,但
髓系树突状细胞不表达TLR9 ,该受体的甲基CpG基序中有丰富的细菌DNA .基因差异决定组成树突状细胞亚群,可能有相关性和敏感性,以感染特定病原体.和谐这一建议,它已经表明,从小鼠树突状细胞的抗感染李斯特菌优先表达TLR9 ,连同树突状细胞的成熟标志CD40分子和CD86 ,并产生高水平的IL - 12的,而树突状细胞从易感小鼠强烈表示TLR2 , -4 , -5和-6 ,并产生大量的趋化蛋白-1 (刘等人. , 2002年) .细胞内信号途径激活受体参与招聘细胞质接头分子MyD88 ,激活的丝氨酸/苏氨酸激酶的义IRAK家庭,并最终降解IkB和易位的NF - kB的核(彰等人. , 2001年) .最近, MyD88依赖性途径已被证明是负责的诱导干扰素- B和干扰素诱导基因(明, 2003年) .在小鼠体内缺乏MyD88 ,东道国抗感染细胞原生动物弓形虫和寄生虫引起的IL - 12的生产树突状细胞被证明是大大减少( Scanga等. ,
2002年) .由于树突状细胞的小鼠日?系数在TLR2或Toll样受体4安装正常IL - 12的答复弓形虫抗原,这些受体似乎并不参与IL - 12的回应这种寄生虫.与此相反, TLR2触发已经证明中发挥作用的诱导
细胞因子的糖脂抗原的克氏锥虫(坎波斯等. , 2001年)和纯蛋白衍生物的结核分枝杆菌
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