免疫性血小板减少症患者中RUNX1表达增加。

Increased RUNX1 expression in patients with immune thrombocytopenia.

作者信息

Zhong Xiaomin, Wu Yulu, Liu Yun, Zhu Feng, Li Xiaoqian, Li Depeng, Li Zhenyu, Zeng Lingyu, Qiao Jianlin, Chen Xiaofei, Xu Kailin

机构信息

Department of Medical Oncology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an 223300, China.

Blood Diseases Institute, Xuzhou Medical College, Xuzhou 221002, China.

出版信息

Hum Immunol. 2016 Aug;77(8):687-691. doi: 10.1016/j.humimm.2016.06.004. Epub 2016 Jun 7.

Abstract

Immune thrombocytopenia (ITP) is a heterogeneous autoimmune disease, characterized by dysregulation of cellular immunity. Th17 and associated IL-17 were involved in the pathogenesis of ITP. Runt-related transcription factor 1 (RUNX1), a member of the runt domain-containing family of transcription factors, is required for Th17 differentiation. Whether RUNX1 was involved in the pathogenesis of ITP remains poorly understood. In this study, 30 active ITP patients, 20 ITP in remission and 20 age and gender matched healthy controls were included. Peripheral blood mononuclear cells (PBMCs) were isolated to measure mRNA level of RUNX1 and retinoic acid receptor-related orphan receptor-γt (RORγt) by quantitative real-time PCR and Th17 cells by flow cytometry. Meanwhile, plasma was extracted for measurement of IL-17 level by ELISA. Our results showed a significantly higher expression of RUNX1, RORγt, Th17 cells and plasma level of IL-17 in active ITP patients than that in healthy controls. No differences of expression of RUNX1, RORγt and Th17 cells were observed between remission patients and controls. Furthermore, a significantly positive correlation of RUNX1 with RORγt was found in active ITP patients. In conclusion, RUNX1 was associated with the pathogenesis of ITP possibly through regulation of Th17 cell differentiation and therapeutically targeting it might be a novel approach in ITP treatment.

摘要

免疫性血小板减少症(ITP)是一种异质性自身免疫性疾病,其特征为细胞免疫失调。Th17细胞及相关的白细胞介素-17(IL-17)参与了ITP的发病机制。 runt相关转录因子1(RUNX1)是含runt结构域转录因子家族的成员之一,是Th17细胞分化所必需的。RUNX1是否参与ITP的发病机制仍知之甚少。在本研究中,纳入了30例活动性ITP患者、20例缓解期ITP患者以及20例年龄和性别匹配的健康对照。分离外周血单个核细胞(PBMC),通过定量实时PCR检测RUNX1和视黄酸受体相关孤儿受体γt(RORγt)的mRNA水平,并通过流式细胞术检测Th17细胞。同时,提取血浆,采用酶联免疫吸附测定法(ELISA)检测IL-17水平。我们的结果显示,活动性ITP患者中RUNX1、RORγt、Th17细胞的表达及血浆IL-17水平显著高于健康对照。缓解期患者与健康对照之间,RUNX1、RORγt的表达及Th17细胞数量未观察到差异。此外,在活动性ITP患者中发现RUNX1与RORγt呈显著正相关。总之,RUNX1可能通过调节Th17细胞分化参与ITP的发病机制,针对其进行治疗靶向可能是ITP治疗的一种新方法。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索