FOXP3型
发病机制
免疫学
免疫系统
炎症
生物
包虫病
RAR相关孤儿受体γ
调节性T细胞
转录因子
白细胞介素2受体
T细胞
基因
遗传学
动物
作者
Tuerhongjiang Tuxun,Junhua Wang,Renyong Lin,Jiaoyu Shan,Qinwen Tai,Taoao Li,Jin Zhang,Ji-Xing Zhao,Hao Wen
标识
DOI:10.1111/j.1365-3024.2012.01383.x
摘要
Summary Echinococcosis is a chronic parasitic infectious disease regulated by T‐cell subsets. CD4 + CD25 + FoxP3 + regulatory T (Treg) cells and Th17 cells have been described as two distinct subsets and have the opposite effect on inflammation. Th17/Treg balance controls inflammation and may play an important role in the pathogenesis of immune evasion. To assess whether this balance was broken, we detected Th17/Treg functions in different levels including cell frequencies, related cytokines secretion and key transcription factors in patients with cystic echincoccosis and healthy controls. The results demonstrated that patients with cystic echinococcosis revealed significant increase in peripheral Treg number, related cytokines (IL‐10 and TGF‐β1) and transcription factor (Foxp3) levels and moderate decrease in Th17 number, related cytokines (IL‐17 and IL‐23) and transcription factor (RORγt) levels as compared with controls. Results indicated that Th17/Treg functional imbalance exists in patients with chronic cystic echinococcosis, suggesting a potential role for Th17/Treg imbalance in the pathogenesis of immune evasion in echinococcosis.
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