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T helper 17/regulatory t cell balance and experimental models of peritoneal dialysis-induced damage

机译:T辅助17 /调节t细胞平衡和腹膜透析诱导损伤的实验模型

摘要

Fibrosis is a general complication in many diseases. It is the main complication during peritoneal dialysis (PD) treatment, a therapyfor renal failure disease. Local inflammation and mesothelial to mesenchymal transition (MMT) are well known key phenomenain peritoneal damage during PD. New data suggest that, in the peritoneal cavity, inflammatory changes may be regulated at least inpart by a delicate balance between T helper 17 and regulatory T cells. This paper briefly reviews the implication of the Th17/Tregaxisin fibrotic diseases. Moreover, it compares current evidences described in PD animal experimental models, indicating a lossof Th17/Treg balance (Th17 predominance) leading to peritoneal damage during PD. In addition, considering the new clinicaland animal experimental data, new therapeutic strategies to reduce the Th17 response and increase the regulatory T response areproposed.Thus, future goals should be to develop newclinical biomarkers to reverse this immunemisbalance and reduce peritonealfibrosis in PD.
机译:纤维化是许多疾病的普遍并发症。它是腹膜透析(PD)治疗(肾衰竭疾病的一种疗法)期间的主要并发症。局部发炎和间皮向间质转化(MMT)是PD腹膜损伤中众所周知的关键现象。新数据表明,在腹膜腔内,炎症改变可能至少部分地由T辅助细胞17和调节性T细胞之间的微妙平衡来调节。本文简要回顾了Th17 / Tregaxis在纤维化疾病中的意义。此外,它比较了PD动物实验模型中描述的当前证据,表明Th17 / Treg平衡丧失(Th17优势)导致PD期间腹膜损伤​​。此外,考虑到新的临床和动物实验数据,提出了减少Th17反应和增加调节性T反应的新治疗策略。因此,未来的目标应该是开发新的临床生物标志物以逆转这种免疫失衡并减少PD的腹膜纤维化。

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