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Potential role of viral infection and B cells as a linker between innate and adaptive immune response in systemic lupus erythematosus
Immunologic Research ( IF 3.3 ) Pub Date : 2021-03-30 , DOI: 10.1007/s12026-021-09186-4
Mohadeseh Zarei Ghobadi 1, 2 , Shima Izadi 2 , Majid Teymoori-Rad 2 , Mohammad Farahmand 2 , Sayed-Hamidreza Mozhgani 3, 4 , Negar Labbaf 2 , Fazel Shokri 5 , Sayed Mahdi Marashi 2
Affiliation  

Systemic lupus erythematosus (SLE) is an autoimmune disease that involves several organ systems. Although B cells play a key role in SLE pathogenesis, the mechanisms behind B cell dysregulation in SLE development remained controversial. Finding the modules containing highly co-expressed genes in B cells could explain biological pathways involved in the pathogenesis of SLE, which may further support the reasons for the altered function of B cells in SLE disease. A total of three microarray gene expression datasets were downloaded from Gene Expression Omnibus. SLE samples were prepared from the purified B lymphocyte cells of the patients who have not received immunosuppressive drugs as well as high dose immunocytotoxic therapies or steroids. A weighted gene co-expression network was then constructed to find the relevant modules implicated in the SLE progression. Among 17 identified modules, 3 modules were selected through mapping to STRING and finding the ones that had highly connection at the protein level. These modules clearly indicate the involvement of several pathways in the pathogenesis of SLE including viral infection, adaptive immune response, and innate immune response in B lymphocytes. The WGCN analysis further revealed the co-expressed genes involved in both innate and adaptive immune systems. Mix infections and primary immunodeficiency might also dysregulate B lymphocytes, which may facilitate SLE development. As such, identifying novel biomarkers and pathways in lupus would be of importance.



中文翻译:

病毒感染和 B 细胞在系统性红斑狼疮中作为先天性和适应性免疫反应之间的连接器的潜在作用

系统性红斑狼疮 (SLE) 是一种涉及多个器官系统的自身免疫性疾病。尽管 B 细胞在 SLE 发病机制中起关键作用,但 B 细胞失调在 SLE 发展中的机制仍存在争议。在 B 细胞中发现含有高度共表达基因的模块可以解释参与 SLE 发病机制的生物学途径,这可能进一步支持 B 细胞在 SLE 疾病中功能改变的原因。从 Gene Expression Omnibus 下载了总共三个微阵列基因表达数据集。SLE 样本是从未接受免疫抑制药物以及高剂量免疫细胞毒疗法或类固醇的患者的纯化 B 淋巴细胞中制备的。然后构建加权基因共表达网络以找到与 SLE 进展有关的相关模块。在识别的17个模块中,通过映射到STRING并找到在蛋白质水平上具有高度联系的模块,选择了3个模块。这些模块清楚地表明了 SLE 发病机制中的几种途径的参与,包括病毒感染、适应性免疫反应和 B 淋巴细胞中的先天免疫反应。WGCN 分析进一步揭示了参与先天和适应性免疫系统的共表达基因。混合感染和原发性免疫缺陷也可能使 B 淋巴细胞失调,这可能促进 SLE 的发展。因此,识别狼疮中的新生物标志物和途径将很重要。通过映射到STRING并找到在蛋白质水平上具有高度联系的模块,选择了3个模块。这些模块清楚地表明了 SLE 发病机制中的几种途径的参与,包括病毒感染、适应性免疫反应和 B 淋巴细胞中的先天免疫反应。WGCN 分析进一步揭示了参与先天和适应性免疫系统的共表达基因。混合感染和原发性免疫缺陷也可能使 B 淋巴细胞失调,这可能促进 SLE 的发展。因此,识别狼疮中的新生物标志物和途径将很重要。通过映射到STRING并找到在蛋白质水平上具有高度联系的模块,选择了3个模块。这些模块清楚地表明了 SLE 发病机制中的几种途径的参与,包括病毒感染、适应性免疫反应和 B 淋巴细胞中的先天免疫反应。WGCN 分析进一步揭示了参与先天和适应性免疫系统的共表达基因。混合感染和原发性免疫缺陷也可能使 B 淋巴细胞失调,这可能促进 SLE 的发展。因此,识别狼疮中的新生物标志物和途径将很重要。和 B 淋巴细胞的先天免疫反应。WGCN 分析进一步揭示了参与先天和适应性免疫系统的共表达基因。混合感染和原发性免疫缺陷也可能使 B 淋巴细胞失调,这可能促进 SLE 的发展。因此,识别狼疮中的新生物标志物和途径将很重要。和 B 淋巴细胞的先天免疫反应。WGCN 分析进一步揭示了参与先天和适应性免疫系统的共表达基因。混合感染和原发性免疫缺陷也可能使 B 淋巴细胞失调,这可能促进 SLE 的发展。因此,识别狼疮中的新生物标志物和途径将很重要。

更新日期:2021-03-30
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