系统性红斑狼疮患者外周血单一核细胞趋化因子受体2和3mRNA的表达

Study on the mRNA expressions of CCR2 and CCR3 in PBMC of SLE patients

目的:探讨趋化因子受体(CCR)2及CCR3在系统性红斑狼疮(SLE)患者外周血单一核细胞(PBMC)中的表达及与疾病的相关性。方法:对93例SLE患者和30名健康对照者,应用半定量逆转录(RT)-PCR方法检测其CCR2、CCR3mRNA表达水平,并应用SLE疾病活动性指数评分标准(SLEDAI)对SLE患者进行评分。结果:①9例SLE患者活动期、非活动期及对照组PBMCCCR2与CCR3mRNA表达水平分别为2.989±1.595与2.847±2.400、0.388±0.213与0.585±0.219、0.263±0.157与0.602±0.124,活动期与非活动期、对照组相比差异均有显著性(P值分别为0.013,0.004;0.000,0.007);非活动期与对照组相比差异无显著性(P>0.01)。②SLE患者PBMC中CCR2、CCR3mRNA表达水平与SLEDAI分别作直线相关性分析,CCR2mRNA、CCR3mRNA水平与SLEDAI均呈正相关。③具有肌炎临床表现的SLE患者其PBMCCCR2、CCR3表达水平较无肌炎表现时降低。血小板减少的SLE患者比不具有相应症状者CCR2mRNA表达降低。结论:SLE患者PBMCCCR2、CCR3表达均增加,且与疾病活动性呈正相关,而CCR2、CCR3为表达于Th2细胞的趋化因子受体,提示SLE患者Th2细胞占优势。CCR2可能参与SLE患者肌炎及血小板减少的发生,CCR3参与肌炎发生。

Objective: To assess the mRNA expression of some chemokine receptors (CCR2 and CCR3) on peripheral blood mononuclear cell (PBMC) in active or inactive SLE and their correlation with clinical parameters. Methods: Ninety-three SLE patients and 30 healthy controls were enrolled. PBMC were separated from the peripheral blood. Reverse transcription-polymerase chain reaction (RT-PCR) was used to analyze the mRNA expression of CCR2 and CCR3 in PBMC. The clinical features and laboratory findings were recorded and the activity of SLE was evaluated by SLEDAI (SLE disease activity index). Results: ①The levels of CCR2 and CCR3 expression were significantly increased in the group of active SLE as compared with the inactive SLE and healthy controls (P < 0.05). There was no significant difference between the inactive SLE and the healthy control (P > 0.05). ②The mRNA expression of CCR2 and CCR3 was significantly correlated with SLEDAI. ③The mRNA expression of CCR2 and CCR3 was significantly less in the patients with myositis than that in the patients without the symptom. The mRNA expression of CCR2 was also significantly less in the patients with thrombocytopenia than that in the patients without the symptom. Conclusions: The mRNA expressions of CCR2 and CCR3 in the SLE patients' PBMC are increased and correlated with the activity of SLE, which suggest that Th2 up-regulation plays an important role in pathogenesis of SLE.