类风湿关节炎患者血浆sHLA-G表达及其与Treg细胞的相关性研究

目的探讨类风湿关节炎（rheumatoidarthritis，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＋HLA-G＋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。

Association of Plasma Soluble HLA - G with Treg Cells in Patients with Rheumatoid Arthritis.

Objective To investigate the expression of plasma soluble HLA - G（ sHLA - G） in patients with rheumatoid arthritis （RA） and their associations with Treg cell and clinical features of the disease. Methods We studied 40 RA patients as well as 40 healthy controls. Plasma sHLA - G levels were determined by enzyme - linked immunosorbent assay. The fraction of circulating CD3 ~ HLA - G ＋ T cells and CD4 ＋ CD25 ＋ Foxp3 ＋ Treg cells were analyzed by flow cytometry. Results RA patients showed a significantly lower concentration of plasma sHLA -G than the control subjects（P 〈0. OO1 ）. The level of CD3 ＋ HLA -G ＋T cells as well as Treg ceils were significantly lower in RA patients than those in the healthy controls（ P 〈 0.01 ）. Spearman analysis showed that the level of sHLA -G but not CD3＋HLA - G＋ T cells was correlated to the fraction of Treg cells. The level of sHLA - G as well as CD3 ＋ HLA - G ＋ T cells were negatively associated with DAS 28 score（ P 〈 0.05） , but not correlated to ESR, CRP, RF, anti -CCP and ANA （P 〉 0.05 ）. Conclu- sion The abnormal expression of plasma sHLA - G detected in RA suggests that they may play an important role in the development of RA. There is a positive correlation between the levels of plasma sHLA - G and the fraction of Treg cells in peripheral blood. There may exist induction and regulation of molecules through the cell signaling pathways between sHLA - G and Treg cells, which can synergically induce and maintain autoimmune tolerance.