经正规驱梅治疗后,梅毒血清固定患者血清反应素滴度可长期呈低滴度不下降。血清固定的发生主要与梅毒分期、血清初始滴度、无症状神经梅毒、苍白螺旋体(Treponema palladium,TP)重复基因型分型和细胞免疫抑制等因素有关。目前梅毒血清...经正规驱梅治疗后,梅毒血清固定患者血清反应素滴度可长期呈低滴度不下降。血清固定的发生主要与梅毒分期、血清初始滴度、无症状神经梅毒、苍白螺旋体(Treponema palladium,TP)重复基因型分型和细胞免疫抑制等因素有关。目前梅毒血清固定的机制不明,研究提示,梅毒血清固定与机体的免疫失衡和免疫抑制有关。从调节性T细胞(regulatory T cells,Tregs)/Th17细胞平衡异常、Toll样受体表达异常、Th1/Th2型细胞因子的失衡、T细胞亚群比例失调及microRNA表达谱的改变等方面,对梅毒血清固定机制的研究进展作一综述。展开更多
A therapeutic preparation of polyclonal human IgG, i.e., intravenous immunoglobulin (IVIg), has been employed to treat several inflammatory and autoimmune disorders. B cells are supposed to be a target of IVIg, but th...A therapeutic preparation of polyclonal human IgG, i.e., intravenous immunoglobulin (IVIg), has been employed to treat several inflammatory and autoimmune disorders. B cells are supposed to be a target of IVIg, but the molecular mechanism is elusive because of the lack of a suitable experimental system. To gain an insight into the beneficial effect of IVIg on B cells, we first established an experimental setting in which IVIg modulates a murine B cell function in vitro, and then aimed at identifying the mechanistic features at the molecular level. Here we show that IVIg down-regulates IL-10 production by CpG-activated B cells in vitro. The responsible component of IVIg was identified as the F(ab’)2 portion, whose polyclonality is mandatory for the suppressive effect. IVIg, bound to the surface of activated B cells, was found to be co-localized with intracellular SHP-1 on confocal laser microscopy, suggesting that B cell-surface immunoreceptor tyrosine-based inhibitory motif-harboring receptors that recruit SHP-1 are target molecules for IVIg in our experimental setting. Overall, we postulate a scenario in which IVIg attenuates B cells by suppressing IL-10 production, a B cell growth factor, and thus down-regulates the production of pathogenic antibodies.展开更多
文摘经正规驱梅治疗后,梅毒血清固定患者血清反应素滴度可长期呈低滴度不下降。血清固定的发生主要与梅毒分期、血清初始滴度、无症状神经梅毒、苍白螺旋体(Treponema palladium,TP)重复基因型分型和细胞免疫抑制等因素有关。目前梅毒血清固定的机制不明,研究提示,梅毒血清固定与机体的免疫失衡和免疫抑制有关。从调节性T细胞(regulatory T cells,Tregs)/Th17细胞平衡异常、Toll样受体表达异常、Th1/Th2型细胞因子的失衡、T细胞亚群比例失调及microRNA表达谱的改变等方面,对梅毒血清固定机制的研究进展作一综述。
文摘A therapeutic preparation of polyclonal human IgG, i.e., intravenous immunoglobulin (IVIg), has been employed to treat several inflammatory and autoimmune disorders. B cells are supposed to be a target of IVIg, but the molecular mechanism is elusive because of the lack of a suitable experimental system. To gain an insight into the beneficial effect of IVIg on B cells, we first established an experimental setting in which IVIg modulates a murine B cell function in vitro, and then aimed at identifying the mechanistic features at the molecular level. Here we show that IVIg down-regulates IL-10 production by CpG-activated B cells in vitro. The responsible component of IVIg was identified as the F(ab’)2 portion, whose polyclonality is mandatory for the suppressive effect. IVIg, bound to the surface of activated B cells, was found to be co-localized with intracellular SHP-1 on confocal laser microscopy, suggesting that B cell-surface immunoreceptor tyrosine-based inhibitory motif-harboring receptors that recruit SHP-1 are target molecules for IVIg in our experimental setting. Overall, we postulate a scenario in which IVIg attenuates B cells by suppressing IL-10 production, a B cell growth factor, and thus down-regulates the production of pathogenic antibodies.
