重症肌无力病病理生物学中与 Th17 通路相关的免疫特征:整合调节/效应细胞因子和转录因子的作用

Q4 Immunology and Microbiology
Nibu Varghese, M. Nagappa, N. Sreenivas, Saikat Dey, T. Mullapudi, Anagha Pettututhazhe Kuniyil, S. Shivaram, D. Seshagiri, B. V. Nair, M. Debnath
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引用次数: 0

摘要

重症肌无力(MG)是一种自身免疫性疾病,由针对乙酰胆碱受体(AChR)、肌肉特异性激酶(MuSK)和神经肌肉接头处其他抗原的抗体介导。抗体的产生受 T 淋巴细胞的影响。T辅助细胞17(Th17)亚群是Th细胞的炎症系,与多种自身免疫性疾病有关。据报道,在 MG 中,T 淋巴细胞与致病性抗体反应(包括异常的 Th17 细胞反应)之间存在功能性相互作用。然而,Th17 细胞活化和/或致病性转化的确切机制尚不清楚。本研究旨在同时探究MG患者Th17细胞的诱导因子、主调节转录因子和效应因子的作用。在这项横断面研究中,采用定量聚合酶链式反应(qPCR)对 59 名 MG 患者和 61 名健康对照者的外周单核细胞中 IL6、IL17A、STAT3 和 RORC 的基因表达进行了定量,并采用多重悬浮检测法估测了血浆中 IL-1β、IL-6 和 IL-17A 细胞因子的水平。与健康对照组相比,患者血浆中的 IL-1β、IL-6 和 IL-17A 水平明显升高。IL17A和RORC基因表达与临床特征相关。本研究证实了 Th17 通路在 MG 病理生物学中的关键作用,包括其对疾病严重程度的潜在影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Th17 pathway‐related immune signatures in the pathobiology of myasthenia gravis: Integrating the roles of regulatory/effector cytokines and transcription factors
Myasthenia gravis (MG) is an autoimmune disorder mediated by antibodies against the acetylcholine receptor (AChR), muscle specific kinase (MuSK), and other antigens in the neuromuscular junction. Antibody production is influenced by T lymphocytes. The T helper 17 (Th17) subset, an inflammatory lineage of Th cells, is associated with several autoimmune diseases. Functional interactions between T lymphocytes and pathogenic antibody responses including aberrant Th17 cell responses have been reported in MG. However, the precise mechanism(s) underlying the activation and/or pathogenic transformation of Th17 cells are not clearly known. The current study aimed at simultaneously exploring the roles of the inducers, master regulator transcription factors, and effectors of Th17 cells in patients with MG.In this cross‐sectional study, quantification of gene expression of IL6, IL17A, STAT3, and RORC in the peripheral mononuclear cells by quantitative polymerase chain reaction (qPCR) as well as estimation of plasma levels of IL‐1β, IL‐6, and IL‐17A cytokines by multiplex suspension assay were carried out in 59 patients with MG and 61 healthy controls.Gene expression levels of IL17A were significantly upregulated in patients as compared to healthy controls. The plasma levels of IL‐1β, IL‐6, and IL‐17A were significantly elevated in patients compared to healthy controls. IL17A as well as RORC gene expressions correlated with the clinical features. IL17A gene expression levels were higher in AChR‐MG patients.The present study supports the crucial role of the Th17 pathway in the pathobiology of MG, including its potential influence on disease severity.
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来源期刊
Clinical and Experimental Neuroimmunology
Clinical and Experimental Neuroimmunology Immunology and Microbiology-Immunology and Microbiology (miscellaneous)
CiteScore
1.60
自引率
0.00%
发文量
52
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