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To the Editor:We thank Trinath et al for their interest in our recently published data on the mechanism of action of intravenous immuno-globulin (IVIg) using our model of allergic airways disease. We demonstrated that allergic airway hyperresponsiveness was abrogated by IVIg via induction of allergen-specific regulatory T cells. The induction of regulatory T cells was dependent on the presence of antigen (ovalbumin [OVA] or ragweed) and could be duplicated by adoptive transfer of dendritic cells (DCs) from mice treated with IVIg. In analyzing both lung digests and isolated pulmonary DCs, we found high Jagged-1 expression following OVA exposure, which was reversed by IVIg. In addition, DCs from OVA-exposed, IVIg-treated mice exhibited increases in Delta-4 expression. Regulatory T-cell induction via modulation of Notch-ligand expression on DCs is one possible explanation for the action of IVIg.
机译:致编辑:我们感谢Trinath等人对我们最近发表的有关使用过敏性气道疾病模型的静脉免疫球蛋白(IVIg)作用机理的数据感兴趣。我们证明,通过诱导过敏原特异性调节性T细胞,IVIg消除了过敏性气道高反应性。调节性T细胞的诱导取决于抗原(卵清蛋白[OVA]或豚草)的存在,并且可以通过过继转移IVIg处理小鼠的树突状细胞(DC)来复制。在分析肺部消化物和分离的肺部DC时,我们发现OVA暴露后高Jagged-1表达,这被IVIg逆转。另外,来自OVA暴露,经IVIg处理的小鼠的DC显示出Delta-4表达增加。通过调节DC上的Notch-配体表达来调节T细胞是IVIg作用的一种可能解释。

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