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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Semaphorin 3A: Is a key player in the pathogenesis of asthma
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Semaphorin 3A: Is a key player in the pathogenesis of asthma

机译:Semaphorin 3a:是哮喘发病机制的关键球员

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摘要

Abstract Immune semaphorins are key players in regulating immune mediated inflammation. Semaphorin3A (sema3A) a secreted and membrane bound member of this family, is well reported for its properties in maintaining self-tolerance. Semaphorin3A was recognized to be a marker for T-regulatory cells (Tregs), and as such is a useful tool for assessing the status of these cells in preventing immune mediated diseases. This study was designed aiming to evaluate how sema3A is possibly involved in bronchial asthma. Here, we found sema3A serum levels and the expression of sema3A on Tregs significantly lower in patients with moderate to severe asthma when compared to healthy individuals. Co-culture of condition medium with 2mcg/ml of recombinant human sema3A with CD4+ T cells, increased the expression of FoxP3 in Tregs, suggesting sema3A a potent immune-regulator of inflammation including that of asthma. Further in-vivo studies will better establish the beneficial effect of sema3A in regulating inflammation in asthma. Highlights ? Sema3A serum levels are decreased in asthma patients. ? Lower levels of sema3A are in correlation with asthma severity. ? T regulatory cells are important in suppressing airway inflammation. ? The expression of sema3A on T regulatory cells is decreased in asthma. ? Co-culture of sema3A with T regulatory cells increases the expression of FoxP3.
机译:摘要免疫信号素是调节免疫介导的炎症的关键球员。 Semaphorin3a(Sema3a)该家庭的分泌和膜结合成员,在保持自我容忍方面是其性质的良好报道。 Semaphorin3a被认为是T-调节细胞(Tregs)的标志物,因此是一种有用的工具,用于评估预防免疫介导的疾病的这些细胞的状态。本研究旨在评估Sema3a如何涉及支气管哮喘。在这里,我们发现Sema3a血清水平和在与健康个体相比时,中度至严重哮喘的患者显着降低了Sema3a对Tregs的表达显着降低。用2mcg / ml重组人Sema3a与CD4 + T细胞的病症培养基的共培养,增加了Foxp3在Tregs中的表达,表明Sema3a具有哮喘的炎症的有效免疫调节剂。进一步的体内研究将更好地建立Sema3a在哮喘中调节炎症的有益作用。强调 ?在哮喘患者中,SEMA3A血清水平降低。还较低水平的Sema3a与哮喘严重程度相关。还T调节细胞对于抑制气道炎症是重要的。还SEMA3A对T调节细胞的表达在哮喘中降低。还SEMA3A与T调节细胞的共培养增加了FOXP3的表达。

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