Hagiwara H, Huang H J, Arai N, Herzenberg L A, Arai K, Zlotnik A
J Immunol. 1987 Apr 15;138(8):2514-9.
We have investigated the mechanism of action of IL 1 on T cell activation. For this purpose, we analyzed the content of specific messenger RNA for lymphokines and other genes that are associated with T cell activation in the murine IL 1-dependent T cell lymphoma LBRM33-1A5. Using cloned genes for IL 2, IL 3, TGF-beta, TY5, IL 2 receptor, Ly-1, c-myc, and p53 as probes in the S1 nuclease protection assay, we compared the amount of specific transcripts among total RNA prepared from unstimulated cells, IL 1 alpha or PHA-stimulated cells, and PHA plus IL 1 alpha-stimulated cells. IL 1 alpha augmented the PHA-induced accumulation of IL 2 mRNA with a magnitude comparable to the amount of IL 2 produced, suggesting that IL 1 alpha modulates IL 2 gene expression at the RNA level. Similar results were obtained with IL 3. We also observed that Ly-1 mRNA appears after PHA treatment and its accumulation was augmented by IL 1 alpha addition. On the basis of the effects of IL 1 alpha and/or PHA treatments on gene expression, we classified these genes into four groups. In all cases, IL 1 alpha seemed to affect mRNA levels quantitatively. These observations support previously described characteristics of this cytokine as a co-stimulator of T cell activation.
我们研究了白细胞介素1(IL-1)对T细胞激活的作用机制。为此,我们分析了小鼠IL-1依赖的T细胞淋巴瘤LBRM33-1A5中与T细胞激活相关的淋巴因子和其他基因的特异性信使核糖核酸(mRNA)含量。在S1核酸酶保护试验中,使用白细胞介素2(IL-2)、白细胞介素3(IL-3)、转化生长因子-β(TGF-β)、TY5、IL-2受体、Ly-1、原癌基因c-myc和抑癌基因p53的克隆基因作为探针,我们比较了从未刺激细胞、IL-1α或PHA刺激细胞以及PHA加IL-1α刺激细胞中制备的总RNA中特异性转录本的量。IL-1α增强了PHA诱导的IL-2 mRNA积累,其幅度与产生的IL-2量相当,表明IL-1α在RNA水平上调节IL-2基因表达。IL-3也得到了类似的结果。我们还观察到,Ly-1 mRNA在PHA处理后出现,并且添加IL-1α会增强其积累。根据IL-1α和/或PHA处理对基因表达的影响,我们将这些基因分为四组。在所有情况下,IL-1α似乎在数量上影响mRNA水平。这些观察结果支持了先前描述的这种细胞因子作为T细胞激活共刺激因子的特征。