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机构地区:[1]南京医科大学第二附属医院心内科,210011
出 处:《免疫学杂志》2010年第7期602-605,611,共5页Immunological Journal
基 金:2007年度南京医科大学科技发展基金面上项目(07NMUM045)
摘 要:目的探讨Toll样受体(Toll-like receptor,TLR)介导丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)信号转导在体外对急性心肌梗塞(acute myocardial infarction,AMI)患者树突状细胞(dendritic cell,DC)的功能影响。方法将去年我院住院患者分3组:AMI组、稳定性心绞痛(stable pectoris,SP)组及正常对照组,各自从外周血中体外培养DC,各组DC分别应用流式细胞仪检测细胞表面TLR及CD80水平,RT-PCR检测TLR的mRNA水平,免疫印迹法检测MAPK家族中p38及JNK水平;HSP60刺激各组DC后分别应用ELISA法检测IL-6及TNF-α水平。结果 AMI组中DC表达TLR及MAPK家族水平、成熟标记物CD80水平、HSP60刺激后IL-6及TNF-α水平均明显升高(P<0.01)。结论 TLR介导MAPK信号转导参与AMI患者DC的活化过程。We aimed to investigate the effects of signal transduction of mitogen-activated protein kinase(MAPK) family mediated by Toll-like receptors(TLRs) on the function of dendritic cells(DCs) in patients with acute myocardial infarction(AMI) in vitro.We divided study population into three groups:AMI group,stable pectoris(SP) group,and control group.DCs were incubated in vitro from peripheral blood of all groups,and then we examined the expression of TLR protein and mRNA by flow cytometry and real-time quantitative reverse transcription polymerase chain reaction(RT-PCR).The expression of MAPK family proteins was determined by Western blot analysis.In addition,the expression level of CD80 was examined by flow cytometry.The levels of cytokines,such as IL6 and TNF-α,in DCs of all groups treated with heat shock protein60(HSP60) were compared.We found that the expressions of TLRs and MAPK families(p38 and JNK) were increased in the patients with AMI,compared with that in the patients of SP group and control group(P 0.01).Likewise,the levels of the mature marker(CD80) and cytokines(IL-6 and TNF-α) responding to HSP60 were elevated in AMI group(P 0.01).This study shows that the signal transduction of MAPK family mediated by TLRs is involved in activation of DCs of AMI patients.
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