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作 者:张继云[1] 赵旌[1] 王梅[1] 李文艳[1] Zhang Jiyun;Zhao Jing;Wang Mei;Li Wenyan(Department of Rheumatology and Immunology,the Second Affiliated Hospital of Xinjiang Medical University,Urumqi 830028,China)
机构地区:[1]新疆医科大学第二附属医院风湿免疫科,乌鲁木齐830028
出 处:《中华风湿病学杂志》2018年第12期824-827,共4页Chinese Journal of Rheumatology
基 金:新疆维吾尔自治区自然科学基金(2016D01C194).
摘 要:目的观察RA患者IL-38表达水平变化,并探讨IL-38对辅助性T细胞17(Th17)细胞的影响。方法采用实时荧光定量PCR检测IL-38 mRNA水平;ELISA法检测血清IL-38及IL-17水平;流式细胞术检测外周血Th17细胞数量;采用t检验或Mann-Whitney秩和检验。结果①实时荧光定量PCR结果显示RA患者IL-38基因表达水平(2.9±4.0)低于健康对照组(5.8±3.6),差异有统计学意义(Z=-1.28,P<0.05);RA患者IL-38蛋白表达水平(0.44±0.03)低于健康对照组(0.72±0.58),差异有统计学意义(Z=-1.59,P<0.05);② RA患者外周血Th17细胞数量(11.7±3.2)高于健康对照组(7.9±2.3),差异有统计学意义(Z=-1.98,P<0.05);且Th17细胞数量与IL-38水平呈负相关(r=-0.38,P<0.05);③ RA患者外周血IL-17水平(64±52)高于健康对照组(35±8),差异有统计学意义(Z=-2.17,P<0. 05);且IL-17水平与IL-38浓度呈负相关(r=-0.31,P<0. 05);④在体外实验中,RA患者外周血中加入IL-38后,Th17细胞数量(5.7±1.2)较RA患者明显下降(7.9±2.3),差异有统计学意义(Z=-1.57,P<0.05)。结论RA患者外周血IL-38表达降低,Th17细胞数量及IL-17表达水平增加,并且与IL-38水平呈负相关;在体外实验中,IL-38能够降低Th17细胞数量,推测在RA患者体内IL-38水平下降,造成Th17细胞及相关细胞因子过度活化,从而导致机体免疫异常,引发RA。Objective To investigate the effect of interleukin (IL)-38 on T helper 17 (Th17) cells in patients with rheumatoid arthritis (RA).Methods Total RNA were extracted and reverse transcribed into complementary DNA. Real-time polymerase chain reaction (PCR) technique was used to determine the gene expression of IL-38 at transcription level. Enzyme linked immune sorbent assay (ELISA) was used to detect the levels of IL-38 and IL-17 in peripheral blood. The percentage of peripheral blood Th17 cells was deter-mined by Flow cytometry. Statistical analysis was conducted with t-test and Mann-Whitney U rank test.Results ① IL-38 mRNA expression from RA patients (2.9±4.0) was significantly reduced as compared with normal controls (5.8±3.6), (Z=-1.28, P<0.05). IL-38 protein expression from RA patients (0.44±0.03) was lower than healthy controls (0.72±0.58), (Z=-1.59, P<0.05). ② The number of Th17 cells from RA patients (11.7±3.2) increased compared with healthy controls (7.9±2.3), (Z=-1.98, P<0.05). The counts of Th17 cells from RA patients was negatively correlated with IL-38 (r=-0.38, P<0.05). ③ The level of peripheral blood IL-17 in RA (64±52) was significantly higher than normal controls (35±8), (Z=-2.17, P<0.05). The level of IL-17 in RA was negatively correlated with IL-38 (r=-0.31, P<0.05). ④ IL-38 caused a significant decrease in the number of Th17 cells from RA patients (5.7±1.2) compared with untreated cells (7.9±2.3), (Z=-1.57, P<0.05).Conclusion The decrease of IL-38 level in RA patients has resulted in the excessive activation of Th17 cells, which triggers the occurrence of RA.
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