目的:探讨创伤后脾细胞活化T细胞核因子(nuclear factor of activated T cells,NFAT)和激活蛋白-1(activator protein-1,AP-1)的DNA结合活性、部分家族成员c-Fos,c-Jun,JunB蛋白的表达和白细胞介素2(IL-2)表达的动态变化及它们间的关系...目的:探讨创伤后脾细胞活化T细胞核因子(nuclear factor of activated T cells,NFAT)和激活蛋白-1(activator protein-1,AP-1)的DNA结合活性、部分家族成员c-Fos,c-Jun,JunB蛋白的表达和白细胞介素2(IL-2)表达的动态变化及它们间的关系。方法:采用小鼠双后肢闭合性砸伤+骨折模型,于创伤后6、12h,1、4、7、10、14d处死动物,分离脾细胞,经ConA刺激细胞后收集培养上清以测定IL-2活性;提取脾细胞RNA以测定IL-2 mRNA;提取脾细胞核蛋白,用电泳迁移率改变试验(electrophoretic mobility shift assay,EMSA)检测NFAT、AP-1的DNA结合活性,用免疫蛋白印迹法(Western blot assay)检测c-Fos,c-Jun,JunB蛋白的表达。结果:和正常对照组相比,创伤后IL-2活性均有不同程度的降低,其受抑的程度在创伤后4d更为明显。创伤后脾细胞NFAT和AP-1的DNA结合活性亦逐渐下降,至伤后4d时下降最明显,为正常对照组的41%和49%。这与创伤后脾细胞IL-2的活性和IL-2 mRNA的降低相一致。c-Fos蛋白水平在伤后1、4d明显降低;c-Fos蛋白表达无明显变化;JunB蛋白水平仅在伤后1d明显表达。结论:上述结果提示,创伤后脾细胞IL-2表达受抑至少部分是由于核转录因子NFAT和AP-1的DNA结合活性降低所导致;而NFAT和AP-1的DNA结合活性降低可能部分由于创伤影响c-Fos蛋白的生成所致。展开更多
Previous studies reported the association between interleukin-6(IL-6)-174G/C gene polymorphism and the risk of diabetic nephropathy in type 2 diabetes mellitus(T2DN).However,the results remain controversial.In the pre...Previous studies reported the association between interleukin-6(IL-6)-174G/C gene polymorphism and the risk of diabetic nephropathy in type 2 diabetes mellitus(T2DN).However,the results remain controversial.In the present study,we conducted a meta-analysis to further examine this relationship between IL-6-174G/C gene polymorphism and T2DN.Three databases(PubMed,SinoMed and ISI Web of Science)were used to search clinical case-control studies about IL-6-174G/C polymorphism and T2DN published until Apr.14,2018.Fixed-or random-effects n lodels were used to calculate the effect sizes of odds ratio(OR)and 95%confide nee intervals(95%CI).Moreover,subgroup analysis was performed in tenns of the excretion rate of albuminuria.All the statistical analyses were con ducted using Stata 12.0.A total of 11 case-control studies were included in this study,involving 1203 cases of T2DN and 1571 cases of T2DM without DN.Metaanalysis showed that there was an association between IL-6-174G/C polymorphism and increased risk of T2DN under the allelic and recessive genetic models(G vs.C:OR=1.10,95%CI 1.03-1」&P=0.006;GG vs.CC+GC:OR=1.11,95%CI 1.02-1.21,P=0.016).In the subgroup analysis by albuminuria,a significant association of IL-6-174G/C polymorphism with risk of T2DN was noted in the microalbuminuria group under the recessive model(OR=1.54,95%CI 1.02-2.32,P=0.038).In conclusion,this meta-analysis suggests that IL-6-174G/C gene polymorphism is associated with the risk of T2DN.展开更多
本研究查明白介素2(IL-2)对静息T细胞抗原特异性免疫应答的作用,探讨IL-2对静息T细胞中细胞因子信号传导抑制蛋白(suppressor of cytokine signaling3,SOCS-3)表达的影响,及其与抗原特异性免疫应答的关系。用IL-2(50U/ml)预处理静息DO11...本研究查明白介素2(IL-2)对静息T细胞抗原特异性免疫应答的作用,探讨IL-2对静息T细胞中细胞因子信号传导抑制蛋白(suppressor of cytokine signaling3,SOCS-3)表达的影响,及其与抗原特异性免疫应答的关系。用IL-2(50U/ml)预处理静息DO11.10T细胞,洗涤去除IL-2后用3H-TdR掺入法检测静息DO11.10T细胞针对OVA323-329抗原(ovalbumin,OVA,卵清蛋白)的特异性增殖;用IL-2(50U/ml)刺激静息DO11.10T细胞,然后用荧光实时定量PCR法检测SOCS-3在刺激后不同时间的表达变化;用OVA323-329抗原活化静息DO11.10T细胞,然后检测SOCS-3在抗原活化后不同时间的表达变化。结果表明:静息DO11.10T细胞经IL-2刺激后抗原特异性增殖能力减弱;静息DO11.10T细胞经IL-2刺激后SOCS-3表达上调,在刺激4小时后表达即明显上调,6小时后达到最高峰;静息DO11.10T细胞经OVA323-329抗原活化后SOCS-3表达明显下调,在活化后第2天降至最低,4天后基本恢复正常。结论:IL-2在一定条件下可抑制静息T细胞抗原特异性免疫应答,而且这种抑制作用可能与SOCS-3表达上调有关。展开更多
文摘目的:探讨创伤后脾细胞活化T细胞核因子(nuclear factor of activated T cells,NFAT)和激活蛋白-1(activator protein-1,AP-1)的DNA结合活性、部分家族成员c-Fos,c-Jun,JunB蛋白的表达和白细胞介素2(IL-2)表达的动态变化及它们间的关系。方法:采用小鼠双后肢闭合性砸伤+骨折模型,于创伤后6、12h,1、4、7、10、14d处死动物,分离脾细胞,经ConA刺激细胞后收集培养上清以测定IL-2活性;提取脾细胞RNA以测定IL-2 mRNA;提取脾细胞核蛋白,用电泳迁移率改变试验(electrophoretic mobility shift assay,EMSA)检测NFAT、AP-1的DNA结合活性,用免疫蛋白印迹法(Western blot assay)检测c-Fos,c-Jun,JunB蛋白的表达。结果:和正常对照组相比,创伤后IL-2活性均有不同程度的降低,其受抑的程度在创伤后4d更为明显。创伤后脾细胞NFAT和AP-1的DNA结合活性亦逐渐下降,至伤后4d时下降最明显,为正常对照组的41%和49%。这与创伤后脾细胞IL-2的活性和IL-2 mRNA的降低相一致。c-Fos蛋白水平在伤后1、4d明显降低;c-Fos蛋白表达无明显变化;JunB蛋白水平仅在伤后1d明显表达。结论:上述结果提示,创伤后脾细胞IL-2表达受抑至少部分是由于核转录因子NFAT和AP-1的DNA结合活性降低所导致;而NFAT和AP-1的DNA结合活性降低可能部分由于创伤影响c-Fos蛋白的生成所致。
文摘Previous studies reported the association between interleukin-6(IL-6)-174G/C gene polymorphism and the risk of diabetic nephropathy in type 2 diabetes mellitus(T2DN).However,the results remain controversial.In the present study,we conducted a meta-analysis to further examine this relationship between IL-6-174G/C gene polymorphism and T2DN.Three databases(PubMed,SinoMed and ISI Web of Science)were used to search clinical case-control studies about IL-6-174G/C polymorphism and T2DN published until Apr.14,2018.Fixed-or random-effects n lodels were used to calculate the effect sizes of odds ratio(OR)and 95%confide nee intervals(95%CI).Moreover,subgroup analysis was performed in tenns of the excretion rate of albuminuria.All the statistical analyses were con ducted using Stata 12.0.A total of 11 case-control studies were included in this study,involving 1203 cases of T2DN and 1571 cases of T2DM without DN.Metaanalysis showed that there was an association between IL-6-174G/C polymorphism and increased risk of T2DN under the allelic and recessive genetic models(G vs.C:OR=1.10,95%CI 1.03-1」&P=0.006;GG vs.CC+GC:OR=1.11,95%CI 1.02-1.21,P=0.016).In the subgroup analysis by albuminuria,a significant association of IL-6-174G/C polymorphism with risk of T2DN was noted in the microalbuminuria group under the recessive model(OR=1.54,95%CI 1.02-2.32,P=0.038).In conclusion,this meta-analysis suggests that IL-6-174G/C gene polymorphism is associated with the risk of T2DN.
文摘本研究查明白介素2(IL-2)对静息T细胞抗原特异性免疫应答的作用,探讨IL-2对静息T细胞中细胞因子信号传导抑制蛋白(suppressor of cytokine signaling3,SOCS-3)表达的影响,及其与抗原特异性免疫应答的关系。用IL-2(50U/ml)预处理静息DO11.10T细胞,洗涤去除IL-2后用3H-TdR掺入法检测静息DO11.10T细胞针对OVA323-329抗原(ovalbumin,OVA,卵清蛋白)的特异性增殖;用IL-2(50U/ml)刺激静息DO11.10T细胞,然后用荧光实时定量PCR法检测SOCS-3在刺激后不同时间的表达变化;用OVA323-329抗原活化静息DO11.10T细胞,然后检测SOCS-3在抗原活化后不同时间的表达变化。结果表明:静息DO11.10T细胞经IL-2刺激后抗原特异性增殖能力减弱;静息DO11.10T细胞经IL-2刺激后SOCS-3表达上调,在刺激4小时后表达即明显上调,6小时后达到最高峰;静息DO11.10T细胞经OVA323-329抗原活化后SOCS-3表达明显下调,在活化后第2天降至最低,4天后基本恢复正常。结论:IL-2在一定条件下可抑制静息T细胞抗原特异性免疫应答,而且这种抑制作用可能与SOCS-3表达上调有关。
