FOXP3型
发病机制
免疫学
医学
视神经脊髓炎
多发性硬化
免疫系统
外周血单个核细胞
周边公差
调节性T细胞
自身免疫
T细胞
白细胞介素2受体
生物
遗传学
体外
作者
Livnat Brill,Iris Lavon,Adi Vaknin‐Dembinsky
标识
DOI:10.1016/j.msard.2019.01.047
摘要
Alterations in the frequency or function of regulatory T cells (Tregs), which play a critical role in the maintenance of peripheral immune tolerance, are known to be involved in the pathogenesis of several autoimmune diseases. Neuromyelitis optica spectrum disorders (NMOSD) are autoimmune inflammatory diseases of the central nervous system (CNS), of which the etiology and mechanisms underlying its development are not completely understood. Although there is increasing evidence for the involvement of effector T cells in NMOSD, no data are available regarding the role of Tregs in its pathogenesis.The aim of this study was to investigate the mRNA expression level of regulatory T cell genes in NMOSD.We used gene expression array and RT-PCR analysis to study Treg cell genes in NMOSD RESULTS: A distinctive Treg gene signature in the peripheral blood of NMOSD patients is described, as well as significantly decreased FoxP3 mRNA expression in the peripheral blood mononuclear cells (PBMCs) of the patients vs that in the healthy controls (HCs) (NMOSD,1.8RQ vs HC, 6.8RQ, p = 0.01).The present study shows downregulation at the mRNA expression level of a Treg key transcription factor FoxP3, in NMOSD. Exploration of Tregs function and interconnections in the peripheral immune system should advance our understanding of NMOSD pathogenesis.
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