摘要
本文选择钙离子导游剂A23187、PKC酶激活物TPA、钙通道阻拮剂Verapamil和钙调素拮抗剂Chloropromazine,以PHA诱导人外周血单核细胞产生IFN-γ为反应体系,观察对细胞内游离钙、细胞增殖和IFN-γ诱生的影响,结果表明PHA、A23187可使得PBMC内游离钙快速增加,通过Quin-2的细胞标记可见荧光光谱的改变,但这种增加或改变可被Verapamil和钙离子螯合剂EGTA所抑制。A23187、TPA可以增强PHA诱生IFN-γ的能力,二者具有协同作用,同样这种效应亦能被Verapamil所抑制。用钙调素拮抗剂Chloripromazine也观察到其对IFN-r诱生的负调节效应。研究的结果还表明对于PHA诱导的细胞增殖效应,A23187、TPA具有增强作用,而Verapamil、Chloropromazine则有抑制效应。据此肯定了T细胞活化、活化信号和IFN-γ诱生的链式反应模式。
We have studied the effects of calcium ionophore A23187, PKC activator TPA, calcium entry blocker verapamil and calmodulin antagonist chloropromazine on the IFN-γ production in the PHA stimulated human peripheral blood mononuclear cell (PBMC) cultures. The results demonstated that human cytosolic free calcium can be increased significantly by PHA and A23187, but this increase can be inhibited by verapamil. We also found that the production of Hu-IFNγ induced by PHA is affected by alteration in calcium flux; both A23187 and TPA could strongly induce the production of IFN-γ, they acted synergistically. This effect was inhibited by 1 mM verapamil. In this paper, \ve used calmodulin antagonist chlopromazine to observe its effect on the Hu-IFNγ production. The results showed that IFN-γ induction can be inhibited by neither pretreatment nor during treatment of this drug. The results also indicated A23187 and TPA can enhance the effect of PHA induced cell proliferation, but verapamil and chloropromazine can inhibit it. On the basis of these results,
we proposed the chain reaction modle: T cell activation-T cell signal-Hu-IFNγ
induction.
出处
《免疫学杂志》
CAS
CSCD
北大核心
1992年第2期95-98,共4页
Immunological Journal
关键词
T细胞活化
细胞内游离钙
T cell activation, Cytosolic free calcium, Calmodulin, Hu-IFNγ induction
