首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Pam3CSK4 enhanced beta cell loss and diabetogenesis: The roles of IFN-gamma and IL-17
【24h】

Pam3CSK4 enhanced beta cell loss and diabetogenesis: The roles of IFN-gamma and IL-17

机译:Pam3CSK4增强β细胞丢失和糖尿病形成:IFN-γ和IL-17的作用

获取原文
获取原文并翻译 | 示例
           

摘要

Toll like receptors are primary sensors of both innate and adaptive immune systems. They activate APCs and influence T-cell function in inflammatory autoimmune response. Studies have shown that TLR manipulation may lead to either tolerance or trigger autoimmunity. Using diabetogenic and subdiabetogenic multiple low doses of streptozotocin, we demonstrate here that Pam3 CYS-CK4 a TLR-2 agonist, enhances and promotes diabetes in C57BL/6 male mice following increased apoptosis of β islet cells. FACS analysis of isolated pancreatic lymph node cells revealed significant increased number of macrophages, dendritic cells, CD4+ TNF-α+, CD4+ IFN-γ+ and most significantly, CD4+ IL-17+ and reduced number of CD25+Fox p3+ T cells after Pam3CSK4 treatment. Genetic deletion of IFN-γ prevents whereas deletion of IL-17 reduced severity of Pam3CSK4-induced enhancement of diabetes. TLR-2 agonist-enhanced diabetogenesis is also influenced by enhanced influx of antigen presenting cells and suppression of regulatory T cell activity.
机译:Toll样受体是先天和适应性免疫系统的主要传感器。它们激活APC并影响炎症性自身免疫反应中的T细胞功能。研究表明,TLR操作可能导致耐受或触发自身免疫。使用成糖尿病和亚糖尿病的多次低剂量链脲佐菌素,我们在这里证明Pam3 CYS-CK4是TLR-2激动剂,在β胰岛细胞凋亡增加后,在C57BL / 6雄性小鼠中增强和促进糖尿病。分离的胰腺淋巴结细胞的FACS分析显示,Pam3CSK4后巨噬细胞,树突状细胞,CD4 +TNF-α+,CD4 +IFN-γ+的数量显着增加,最显着的是CD4 + IL-17 +和CD25 + Fox p3 + T细胞的数量减少治疗。 IFN-γ的基因缺失可防止IL-17的缺失降低Pam3CSK4诱导的糖尿病增强的严重性。 TLR-2激动剂增强的糖尿病发生也受到抗原呈递细胞流入量增加和调节性T细胞活性抑制的影响。

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