Background. As a multifaceted disease, atherosclerosis is often characterized by the formation and accumulation of plaque anchored to the inner wall of the arteries and causes some cardiovascular diseases and vascular embolism. Numerous studies have reported on the pathogenesis of atherosclerosis. However, fewer studies focused on both genes and immune cells, and the correlation of genes and immune cells was evaluated via comprehensive bioinformatics analyses. Methods. 29 samples of atherosclerosis-related gene expression profiling, including 16 human advanced atherosclerosis plaque (AA) and 13 human early atherosclerosis plaque (EA) samples from the Gene Expression Omnibus (GEO) database, were analyzed to get differentially expressed genes (DEGs) and the construction of protein and protein interaction (PPI) networks. Besides, we detected the relative fraction of 22 immune cell types in atherosclerosis by using the deconvolution algorithm of “cell type identification by estimating relative subsets of RNA transcripts (CIBERSORT).” Ultimately, based on the significantly changed types of immune cells, we executed the correlation analysis between DEGs and immune cells to discover the potential genes and pathways associated with immune cells. Results. We identified 17 module genes and 6 types of significantly changed immune cells. Correlation analysis showed that the relative percentage of T cell CD8 has negative correlation with the C1QB expression (, ), and the relative percentage of macrophage M2 has positive correlation with the CD86 expression (, ) in EA. Meanwhile, four gene expressions (CD53, C1QC, NCF2, and ITGAM) have a high correlation with the percentages of T cell CD8 and macrophages (M0 and M2) in AA samples. Conclusions. In this study, we suggested that the progression of atherosclerosis might be related to CD86, C1QB, CD53, C1QC, NCF2, and ITGAM and that it plays a role in regulating immune-competent cells such as T cell CD8 and macrophages M0 and M2. These results will enable studies of the potential genes associated with immune cells in the progression of atherosclerosis, as well as provide insight for discovering new treatments and drugs.

中文翻译：

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综合生物信息学分析发现与动脉粥样硬化进展中的免疫细胞相关的六基因特征。

背景。作为一种多方面的疾病，动脉粥样硬化通常以锚定于动脉内壁的斑块的形成和积累为特征，并导致一些心血管疾病和血管栓塞。许多研究报道了动脉粥样硬化的发病机制。然而，同时关注基因和免疫细胞的研究较少，并且通过综合生物信息学分析评估基因和免疫细胞的相关性。方法。对来自基因表达综合数据库（GEO）的29个动脉粥样硬化相关基因表达谱样本进行分析，包括16个人类晚期动脉粥样硬化斑块（AA）和13个人类早期动脉粥样硬化斑块（EA）样本，以获得差异表达基因（DEG）和蛋白质和蛋白质相互作用（PPI）网络的构建。此外，我们利用“通过估计RNA转录本的相对子集来识别细胞类型（CIBERSORT）”的反卷积算法检测了22种免疫细胞类型在动脉粥样硬化中的相对分数。最终，根据免疫细胞类型的显着变化，我们进行了DEG与免疫细胞之间的相关性分析，以发现与免疫细胞相关的潜在基因和通路。结果。我们鉴定了 17 个模块基因和 6 种显着改变的免疫细胞。相关分析显示，T细胞CD8的相对百分比与C1QB的表达量呈负相关（, ），巨噬细胞M2的相对百分比与CD86表达呈正相关（, ）在 EA 中。同时，四种基因（ CD53、 C1QC、 NCF2和ITGAM）的表达与AA样本中T细胞CD8和巨噬细胞（M0和M2）的百分比具有高度相关性。结论。在这项研究中，我们认为动脉粥样硬化的进展可能与CD86、 C1QB、 CD53、 C1QC、 NCF2和ITGAM有关，并且它在调节T细胞CD8和巨噬细胞M0和M2等免疫活性细胞中发挥作用。这些结果将有助于研究与动脉粥样硬化进展中的免疫细胞相关的潜在基因，并为发现新的治疗方法和药物提供见解。