| 陆军勤,顾光学,于洪威,等.杀伤细胞凝集素样受体 B1对类风湿关节炎外周血 CD8+T细胞功能的影响[J].安徽医药,2024,28(11):2217-2221. |
| 杀伤细胞凝集素样受体 B1对类风湿关节炎外周血 CD8+T细胞功能的影响 |
| Effects of CD161 on peripheral blood CD8+T cell function in patients with rheumatoid arthritis |
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| DOI：10.3969/j.issn.1009-6469.2024.11.021 |
| 中文关键词: NK细胞凝集素样受体亚家族 B CD8+T细胞 记忆细胞 类风湿关节炎 |
| 英文关键词: NK cell lectin-like receptor subfamily B CD8+ T cells Memory cells Rheumatoid arthritis |
| 基金项目:安徽省自然科学基金项目( 2208085MH212)；连云港市第一人民医院青年英才基金项目( QN2304) |
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| 中文摘要: |
| 目的研究杀伤细胞凝集素样受体 B1(CD161)对类风湿关节炎( RA)病人外周血 CD8+T细胞及其亚群功能的影响。方法自 2023年 5―8月，整合基因组学数据库( GEO)不同数据集中对照组及 RA组病人的外周血单细胞数据、 Bulk转录组测序数据及临床相关数据，观察 CD161在对照组及 RA组中的表达差异情况。通过相关性分析指出 CD161与 RA病人临床炎症指标及治疗反应预后的相关性。运用单细胞无监督聚类、细胞注释方法观察 CD161主要表达的细胞亚群及不同细胞亚群在对照组及 RA组中的变化趋势。利用单细胞生物学评分功能计算不同亚群细胞的生物学功能评分，结合基因差异表达分析和功能富集分析，探索 RA病人 CD8+T细胞及其亚群关键生物学功能与 CD161基因表达的潜在关系。结果在人体外周全血中，与对照组相比， RA组中 CD161高表达( 8.779±0.657)(P<0.05)，且 CD161的表达与 RA病人炎症因子 C反应蛋白( CRP，r=?0.21)及血沉( ESR，r=?0.25)呈负相关( P<0.05)。 CD161主要表达于 NK细胞 1.35±0.87、CD4+T细胞 0.62±0.82及 CD8+T细胞 0.85±1.01，但在 CD8+T细胞中表达异质性最显著(标准差 1.01大于平均数 0.85)且 CD161在 CD8+记忆 T细胞中表达丰度最高 1.38±0.34。与对照组相比， RA组中 CD8+T及 CD8+记忆 T细胞频率均下降。与对照，组相比，在 RA病人外周血 CD8+记忆 T细胞中， CD161表达降低( 1.46±0.33比 0.97±0.37，P<0.05)CD161与 CD8+记忆 T细胞迁移( 0.24±0.12比 0.16±0.11)、细胞毒作用( 0.52±0.27比 0.45±0.38)呈正相关(均 P<0.05)与趋化炎能力( 0.15±0.04比 0.17±0.02)呈负相关( P<0.05)，与细胞增殖( 0.02±0.04比 0.03±及促，0.04)或凋亡(0.12±0.22比 0±0.18)相关性差异无统计学意义( P>0.05)。结论 CD161介导 CD8+记忆 T细胞细胞毒作用及促.18，炎功能改变促进 RA发生、发展。 |
| 英文摘要: |
| Objective To investigate the effect of killing cell lectin like receptor B1(CD161) on the function of peripheral blood CD8+ cells and their subsets in patients with rheumatoid arthritis (RA).Methods Peripheral blood single cell genomics data, bulk RNA-seqdata, and clinical related data on the control and RA groups from May to August 2023 were integrated from different datasets of genomics database (GEO) database, and the differential expression of CD161 in the control and RA groups was observed. Through correlationanalysis, the correlation between CD161 and clinical inflammatory indicators and treatment response prognosis in RA patients wasidentified. Single cell unsupervised clustering and cell annotation methods were used to observe the changes in the main and differentcell subsets of CD161 expression in the control group and RA group. The biological function scores of different subsets of cells were calculated by using the single cell biological scoring function, combined with gene differential expression analysis and functional enrichment analysis, the potential relationship between the key biological functions of CD8+ T cells and their subsets and CD161 gene expression in RA patients was explored.Results In the peripheral whole blood of the human body, compared with the control group, CD161was highly expressed in the RA group (8.779±0.657)(P<0.05), and the expression of CD161 was negatively correlated with the inflammatory factor C-reactive protein (CRP, r=?0.21) and erythrocyte sedimentation rate (ESR, r=?0.25) in RA patients (P<0.05). CD161 was mainly expressed in NK cells (1.35±0.87), CD4+ T cells 0.62±0.82, and CD8+ T cells 0.85±1.01, but the heterogeneity of expression was most significant in CD8+ T cells (standard deviation 1.01 greater than mean 0.85), and CD161 had the highest expression abundance in CD8+ memory T cells (1.38±0.34). Compared with the control group, the frequency of CD8+ T and CD8+ memory T cells decreased in the RA group, and CD161 expression was reduced in peripheral blood CD8+ memory T cells of RA patients (1.46±0.33 vs. 0.97±0.37, P<0.05). CD161 was positively correlated with CD8+ memory T cell migration (0.24±0.12 vs. 0.16±0.11) and cytotoxicity (0.52±0.27 vs. 0.45±0.38) (all P<0.05), but negatively correlated with chemotaxis and pro-inflammatory ability (0.15±0.04 vs. 0.17± 0.02) (P<0.05). The correlation with cell proliferation (0.02±0.04 vs. 0.03±0.04) or apoptosis (0.12±0.22 vs. 0.18±0.18) was not statistically significant (P>0.05).Conclusion CD161 mediates the cytotoxic effect of CD8+ memory T cells and changes in pro-inflammatory function, promoting the occurrence and development of RA. |
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