VTRNA2-1在系统性红斑狼疮患者B 细胞中的高表达及其意义

目的： 检测系统性红斑狼疮(systemic lupus erythematosus，SLE)患者中T和B淋巴细胞中穹窿核糖核酸 2-1(vault ribonucleic acid 2-1，VTRNA2-1)基因的表达水平，初步探索SLE的发病机制。方法： 收集25 例健康对照者 和32 例SLE患者的外周血CD4+ T淋巴细胞，另外再收集62 例SLE患者(其中活动性SLE患者47 例，非活动性患者15 例)和29 例健康对照者的外周血CD19+ B淋巴细胞，采用real-time PCR检测VTRNA2-1 基因的表达水平。采用免疫共 沉淀实验寻找VTRNA2-1 的直接作用蛋白。结果： 通过对SLE 患者和健康对照者外周血T 细胞和B 细胞中的 VTRNA2-1 基因进行检测，发现SLE患者T细胞中的VTRNA2-1 基因表达水平与健康对照者相比较，差异无统计学 意义(P>0.05)。活动性和非活动性的SLE患者外周血B细胞中的VTRNA2-1 基因表达水平与健康对照者相比均显著增 高，差异均有统计学意义(分别P<0.01 和P<0.05)。免疫共沉淀实验证实VTRNA2-1 通过与蛋白激酶R(protein kinase R，PKR)特异性结合而发挥生物学功能。结论： VTRNA2-1 基因在SLE患者的B细胞中呈高表达，其机制可能是通 过调控PKR而发挥生物学功能。

High expression of VTRNA2-1 in systemic lupus erythematosus patients’B lymphocytes and its significance

Objective: To investigate the expression of vault ribonucleic acid 2-1 (VTRNA2-1) in T or B lymphocytes in patients with systemic lupus erythematosus (SLE) from the perspective of epigenetic non-coding RNA, and to explore the preliminary pathogenesis of SLE. Methods: CD4+ T lymphocytes from peripheral blood in 25 healthy controls and 32 SLE patients, CD19+ B lymphocytes from peripheral blood in 62 SLE patients (47 patients were active SLE and 15 patients were inactive) and 29 healthy controls were collected, and the expression levels of VTRNA2-1 were detected by real-time PCR. Co-immunoprecipitation assay was used to explore the direct-acting proteins of VTRNA2-1. Results: Through the detection of VTRNA2-1 in peripheral blood T cells and B cells in the SLE patients and healthy controls, we have found that there was no significant difference in the expression of VTRNA2-1 in T cells between the SLE patients and the healthy controls (P> 0.05). The expression of VTRNA2-1 in B cells in the active and inactive SLE patients was both higher than that in the healthy controls, with significant difference (P<0.01 and P< 0.05, respectively). Co-immunoprecipitation assay confirmed that VTRNA2-1 exerted its biological function via specific binding with protein kinase R (PKR). Conclusion: VTRNA2-1 is highly expressed in B cells in the SLE patients, which may play a biological role by regulating PKR.