再生障碍性贫血患者外周血Th17、CD4~+ CD25~+ Treg细胞的免疫应答研究

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目的探究再生障碍性贫血患者外周血TH17、CD4~+ CD25~+ Treg细胞的表达特征及血象影响。方法采集血液标本,进行细胞处理、细胞培养、细胞因子的ELISA检测、流式细胞术检测;将实验结果用Mann-Whitney U秩和检验,进行二分类组间比较;用Kruskal-Wallis H(K)秩和检验,进行多分类趋势分析。结果对照组、NSAA组与SAA组相比,外周血CD4~+ CD25~+ Treg细胞比例依次降低;TH17细胞比例依次升高;差异有统计学意义(P<0.05);TNF-α细胞因子水平组间差异无统计学意义(P>0.05)。SAA组、NSAA组外周血血红蛋白计数与TH17细胞比例均呈负相关(r值分别为-0.09、-0.889,P<0.05)。SAA组、NSAA组外周血血红蛋白计数与CD4~+ CD25~+ Treg细胞比例均呈正相关(r值分别为0.889、0.882,P<0.05)。SAA组、NSAA组外周血血红蛋白计数与血清IL-17细胞因子均呈负相关(r值分别为-0.900、-0.975,P<0.05)。结论 Th17/Treg失衡是再生障碍性贫血发生、发展的关键因素;Th17细胞免疫应答增强,CD4~+ CD25~+ Treg细胞免疫应答减弱,加重了再生障碍性贫血患者骨髓衰竭的严重程度。 Objective To investigate the expression of TH17 and CD4 ~ + CD25 ~ + Treg cells in peripheral blood of patients with aplastic anemia and the influence of hemogram. Methods Blood samples were collected for cell sorting, cell culture, cytokine ELISA and flow cytometry. The results were compared between two groups by Mann-Whitney U rank test. Kruskal-Wallis H (K ) Rank sum test, multi-classification trend analysis. Results Compared with the SAA group, the percentage of CD4 ~ + CD25 ~ + Treg cells in the control group and the NSAA group decreased in turn and the proportion of TH17 cells increased in turn, with statistical significance (P <0.05). The levels of TNF-α and cytokines There was no significant difference between groups (P> 0.05). The counts of peripheral blood hemoglobin in SAA group and NSAA group were negatively correlated with the proportion of TH17 cells (r = -0.09, -0.889, P <0.05, respectively). The counts of peripheral blood hemoglobin in SAA group and NSAA group were positively correlated with the proportion of CD4 ~ + CD25 ~ + Treg cells (r = 0.889,0.882, P <0.05). The counts of peripheral blood hemoglobin in SAA and NSAA groups were negatively correlated with serum IL-17 (r = -0.900, -0.975, P <0.05). Conclusion The imbalance of Th17 / Treg is a key factor in the development of aplastic anemia. The immune response of Th17 cells is enhanced and the immune response of CD4 ~ + CD25 ~ + Treg cells is weakened, which aggravates the severity of bone marrow failure in patients with aplastic anemia.
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