儿童系统性红斑狼疮外周血淋巴细胞表面CTLA-4的表达及意义

目的 探讨外周血淋巴细胞表面CTLA-4在儿童系统性红斑狼疮(SLE)中的表达及意义。 方法 随机选取2012年1月-2015年9月在青岛市妇女儿童医院肾脏免疫科住院治疗的SLE患儿30例为SLE组,其中活动期16例,静止期14例。选择同期健康儿童30例为对照组。应用流式细胞仪技术测定两组外周血T淋巴细胞表面CD28、CTLA-4的表达水平。 结果 SLE组患儿的外周血CD3⁺、CD4⁺及CD8⁺T 细胞上CD28的表达量与对照组比较,差异无统计学意义(均P＞0.05)。SLE组患儿的外周血CD3⁺、CD4⁺及CD8⁺T 细胞上CTLA-4表达均呈低水平,分别为(0.92±0.53)、(0.55±0.41)、(0.57±0.29)。其中SLE组患儿外周血CD3⁺、CD4⁺ T 细胞上CTLA-4分子的表达明显低于对照组(t=3.06、3.11,P＜0.05),CD8⁺T细胞上CTLA-4分子的表达亦低于对照组水平,但差异无统计学意义(t=0.84,P＞0.05)。活动期SLE组患儿外周血CD3⁺、CD4⁺T 细胞上CTLA-4分子的表达(分别为:0.74±0.47、0.41±0.24)明显低于对照组(t=3.40、4.48,均P＜0.05),CD8⁺T细胞上CTLA-4分子(0.47±0.29)的表达亦低于对照组水平(0.65±0.43),但差异无统计学意义(t=1.50,P＞0.05)。静止期SLE组患儿外周血CD3⁺、CD4⁺及CD8⁺T细胞上CTLA-4的表达量均较活动期SLE组患儿升高,且与对照组比较差异无统计学意义(均P＞0.05)。 结论 SLE患儿外周血T 细胞中存在CTLA-4分子表达的缺陷,参与了SLE的发病过程;在SLE发病进展的过程中,CTLA-4表达明显降低,使得免疫反应相对激进,促使疾病的进一步发展。

Expression and significance of CTLA-4 in peripheral blood lymphocytes of children with systematic lupus erythematosus

Objective To explore the expression and value of CTLA-4 in peripheral blood lymphocytes of children with systematic lupus erythematosus (SLE). Methods Thirty children with SLE hospitalized in Department of Pediatric Nephrology, Qingdao Women and Children’s Hospital from January 2012 to September 2015 were randomly selected as SLE group, including 16 cases of active SLE and 14 cases of stationary SLE. 30 healthy children were simultaneously selected as the control group. The expression levels of CD28 and CTLA-4 in peripheral blood T lymphocytes of the 2 groups were tested by flow cytometry. Results No statistically significant difference was found in the expression of CD28 in peripheral blood CD3⁺, CD4⁺ and CD8⁺ T cells between SLE group and the control group (all P>0.05). The expression levels of CTLA-4 in peripheral blood CD3⁺, CD4⁺ and CD8⁺ T cells of SLE group were all low ((0.92±0.53), (0.55±0.41), (0.57±0.29)). The expression of CTLA-4 molecule in peripheral blood CD3⁺ and CD4⁺ T cells of SLE group was significantly lower than that of the control group (t=3.06, t=3.11, P<0.05), and the expression of CTLA-4 molecule in CD8⁺ T cells was also lower than that of the control group, but no statistically significant difference was found (t=0.84, P>0.05). The expression of CTLA-4 molecule in peripheral blood CD3⁺ and CD4⁺ T cells of active SLE group ((0.74±0.47), (0.41±0.24)) was significantly lower than that of the control group (t=3.40, t=4.48, both P<0.05), and the expression of CTLA-4 molecule in CD8⁺ T cells (0.47±0.29) was also lower than that of the control
group (0.65±0.43), but there was no statistically significant difference (t=1.50, P>0.05). The expression levels of CTLA-4 in peripheral blood CD3⁺, CD4⁺ and CD8⁺ T cells of stationary SLE group were all higher than those of active SLE group, but there was no statistically significant difference compared with the control group (all P>0.05). Conclusions There exists a defective expression of CTLA-4 molecule in the peripheral blood T cells from children with SLE; moreover, it is involved in the pathogenesis of SLE. The expression of CTLA-4 is significantly decreased in the pathogenesis and progress of SLE, which induces an active immune response and further development of the disease.