...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cytokine >Insulin-like growth factor-I regulates the neonatal immune response in infection and maturation by suppression of IFN-γ
【24h】

Insulin-like growth factor-I regulates the neonatal immune response in infection and maturation by suppression of IFN-γ

机译：胰岛素样生长因子-I通过抑制IFN-γ调节感染和成熟过程中的新生儿免疫反应

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Disturbances in Insulin-like growth factor-I (IGF-I) and dysregulation in neonatal immune responses have been associated with typical neonatal diseases. Immunosuppression by IGF-I might be a key regulator of neonatal immune responses in infection and maturation. However, information on IGF-I serum levels, IGF-I-receptor (IGF-IR) and effects on functional properties of neonatal immune cells is scarce. Neonatal cord blood samples were stimulated with anti-CD3/anti-CD28, PMA/ionomycin or LPS in a whole-blood assay, while IGF-I serum levels and IGF-I receptor expression were assessed. Furthermore the effect of IGF-I on cytokine expression, apoptosis and the DNA binding activity of AP-1 and NFκB was evaluated. IGF-I serum levels were within normal range. The IGF-I-receptor was present on the surface of cord blood CD3. +. CD4. +. lymphocytes and cord blood CD14. +. monocytes. Upon stimulation the IGF-I-R expression on lymphocytes was significantly upregulated. The addition of IGF-I (100. ng/ml) to whole blood cultures inhibited the secretion of IFN-γ from PMA/ionomycin-stimulated cord blood mononuclear cells (CBMC). While IGF-I did not influence apoptosis in our experimental setting, it led to a distinct decrease in anti-CD3/CD28-stimulated DNA binding activity of AP-1 and NFκB. Thus IGF-I may be a key regulator of neonatal immune responses in maturation processes and inflammation by suppressing proinflammatory Th1 responses. Future in vivo studies need to elucidate whether disturbances of the IGF-I serum level and IGF-IR expression are associated with susceptibility for infections and subsequent diseases in neonates.
机译：胰岛素样生长因子-I（IGF-I）的紊乱和新生儿免疫反应的失调与典型的新生儿疾病有关。 IGF-1的免疫抑制作用可能是感染和成熟过程中新生儿免疫反应的关键调节因子。然而，关于IGF-1血清水平，IGF-1受体（IGF-1R）以及对新生儿免疫细胞功能特性的影响的信息很少。在全血试验中，用抗CD3 /抗CD28，PMA /离子霉素或LPS刺激新生儿脐带血样品，同时评估IGF-1血清水平和IGF-1受体表达。此外，评估了IGF-1对细胞因子表达，细胞凋亡以及AP-1和NFκB的DNA结合活性的影响。 IGF-1血清水平在正常范围内。 IGF-I受体存在于脐带血CD3的表面。 +。 CD4。 +。淋巴细胞和脐带血CD14。 +。单核细胞。刺激后，淋巴细胞上的IGF-I-R表达明显上调。向全血培养物中添加IGF-I（100. ng / ml）会抑制PMA /离子霉素刺激的脐血单核细胞（CBMC）分泌IFN-γ。尽管IGF-I在我们的实验环境中不影响细胞凋亡，但它导致抗CD3 / CD28刺激的AP-1和NFκB的DNA结合活性明显降低。因此，通过抑制促炎性Th1反应，IGF-1可能是成熟过程和炎症中新生儿免疫反应的关键调节剂。未来的体内研究需要阐明IGF-1血清水平和IGF-1R表达的紊乱是否与新生儿感染和随后疾病的易感性有关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号