免疫球蛋白IgG对TNF-α诱导的内皮细胞损伤的作用及其机制  被引量:11

Effects of immunoglobulin IgG in TNF-α-induced endothelial cell damage and the possible mechanism

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作  者:常贺[1] 王焱[1] 李刚[1] 邹军[2] 

机构地区:[1]厦门大学附属中山医院心内科厦门心脏中心,361004 [2]厦门大学医学院基础医学部,361005

出  处:《免疫学杂志》2011年第11期949-953,958,共6页Immunological Journal

基  金:福建省科技计划重点项目(2010Y0053)

摘  要:目的探讨免疫球蛋白IgG对TNF-α诱导的内皮细胞黏附分子、细胞因子的表达及其作用机制。方法不同剂量的免疫球蛋白IgG预处理内皮细胞30 min,再加入TNF-α孵育2 h,或不同剂量的IgG与TNF-α预孵育30 min后加入内皮细胞孵育2 h,RT-PCR及实时定量PCR检测黏附分子ICAM-1、VCAM-1、E-Selectin及细胞因子IL-6、GM-CSF、IFN-β的mRNA表达;进一步应用Western blot检测黏附分子的蛋白表达及免疫球蛋白IgG自身抗体的表达情况。结果 IgG预处理内皮细胞再加入TNF-α或IgG与TNF-α预孵育后加入内皮细胞,IgG均可剂量依赖性地抑制了TNF-α诱导的黏附分子(ICAM-1、VCAM-1、E-Selectin)及细胞因子(IL-6、GM-CSF、IFN-β)的表达,IgG含有anti-IFN-γ,anti-TNF-α,anti-MCP-1的自身抗体。结论 IgG对TNF-α诱导的内皮细胞损伤有治疗作用,其机制与抑制内皮细胞分泌的黏附分子,细胞因子的表达及IgG存在抗细胞因子的自身抗体有关。We aim to explore the effects of Immunoglobulin(IgG) on the expression of adhesion molecules and cytokines in TNF-α-induced endothelial cells(ECs) damage and its possible mechanism.ECs were pretreated with different concentrations IgG for 30 min,and then stimulated with TNF-α for 2 h.Different concentrations of IgG and TNF-α were preincubated for 30 min,and then added to the ECs for 2 h.Then we detected the levels of adhesion molecules(ICAM-1,VCAM-1,E-selectin) and cytokines(IL-6,GM-CSF,IFN-β) by Quantitative Real-time RT-PCR.Furthermore,The expression of adhesion molecules(ICAM-1,VCAM-1,E-selectin) and autoantibodies of IgG were determined by Western blot analysis.We found that IgG does-dependently inhibited the production of adhesion molecules(ICAM-1,VCAM-1,E-selectin) and cytokines(IL-6,GM-CSF,IFN-β) induced by TNF-α.And IgG contained anti-IFN-γ,anti-TNF-α,and anti-MCP-1 autoantibodies.In conclusion,possible regulatory mechanism of IgG on ECs function may associate with adhesion molecules inhibiting,cytokines expression and IgG containing autoantibodies against cytokines.

关 键 词:免疫球蛋白 TNF-Α 内皮细胞 细胞因子 自身抗体 

分 类 号:R392[医药卫生—免疫学]

 

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