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目的探讨类风湿关节炎(rheumatoid arthritis,RA)患者血浆sHLA-G表达水平及其与Treg细胞水平和RA临床特征的相关性。方法选择40例RA患者和40例健康对照者,采用酶联免疫吸附试验(ELISA)法检测血浆sHLA-G表达水平,流式细胞术检测外周血CD3+HLA-G+T细胞、Treg细胞(CD4+CD25+Foxp3+Treg细胞)含量。结果 RA患者血浆sHLA-G水平显著低于健康对照组(P<0.001);RA患者外周血CD3+HLA-G+T细胞百分比明显低于健康对照组(P<0.001);Treg细胞百分比也较对照组明显降低(P<0.01)。相关性分析显示,RA患者Treg细胞百分比与sHLA-G水平存在明显正相关性(P<0.01),而与CD3+HLA-G+T细胞百分比无显著相关(P>0.05);RA患者sHLA-G水平及CD3+HLAG+T细胞百分比均与患者DAS28评分显著负相关(P<0.05),而与患者RF、ESR、CRP、抗CCP抗体和ANA水平等均无明显相关性(P>0.05)。结论 RA患者血浆sHLA-G表达异常降低,其可能参与了RA的发生和疾病进展;血浆sHLA-G水平与外周血Treg细胞百分比呈明显正相关,二者之间可能存在相互诱导和调节的信号途径,在诱导和维持机体自身免疫耐受中起着重要的协同作用。
Objective To investigate the expression of sHLA-G in patients with rheumatoid arthritis (RA) and its correlation with the level of Treg cells and the clinical features of RA. Methods 40 cases of RA patients and 40 healthy controls were selected. The expression of sHLA-G in plasma was detected by enzyme-linked immunosorbent assay (ELISA). The levels of CD3 + HLA-G + T cells and Treg cells in peripheral blood were measured by flow cytometry CD4 + CD25 + Foxp3 + Treg cells) content. Results The level of sHLA-G in RA patients was significantly lower than that in healthy controls (P <0.001). The percentage of CD3 + HLA-G + T cells in RA patients was significantly lower than that in healthy controls (P <0.001) The control group was significantly lower (P <0.01). Correlation analysis showed that the percentage of Treg cells in RA patients was positively correlated with sHLA-G levels (P <0.01), but not with the percentage of CD3 + HLA-G + T cells (P> 0.05) G level and percentage of CD3 + HLAG + T cells were negatively correlated with DAS28 score (P <0.05), but not with RF, ESR, CRP, anti-CCP antibody and ANA levels (P> 0.05) . Conclusion The abnormal expression of sHLA-G in RA patients may be involved in the occurrence and progression of RA. The level of sHLA-G in plasma is positively correlated with the percentage of Treg cells in peripheral blood, and there may be signals of mutual induction and regulation Pathway, plays an important synergistic role in inducing and maintaining the autoimmune tolerance of the body.