A monoclonal antibody to the T-cell receptor increases IGF-I receptor content in normal T-lymphocytes: comparison with phytohemagglutinin.
A monoclonal antibody to the T-cell receptor increases IGF-I receptor content in normal T-lymphocytes: comparison with phytohemagglutinin.
复制标题
T 细胞受体单克隆抗体可增加正常 T 淋巴细胞中 IGF-I 受体的含量：与植物血凝素相比。
DOI：
10.1002/jcb.240480112
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发表时间：
1992
影响因子：
4
通讯作者：
Rosenthal,SM
中科院分区：
文献类型：
--
作者：
Hartmann,KK;Baier,TG;Papa,V;Kronenwett,M;Brown,EJ;Goldfine,ID;Rosenthal,SM
IGFs的生物学效应是通过与特定细胞表面受体的相互作用介导的。以前有报道称植物血凝素（PHA）对T淋巴细胞的有丝分裂激活与IGF - I受体含量的增加有关。然而，在T淋巴细胞活化过程中调节IGF - I受体表达的机制尚不清楚。为了进一步探索IGF - I受体在T细胞中的表达调控，我们研究了在PHA或OKT - 3刺激后T淋巴细胞中IGF - I受体的含量和mRNA丰度，后者是一种针对T细胞受体的CD - 3抗原的单克隆抗体，IGF - I结合在T细胞中，在PHA和OKT - 3刺激后显示IGF - I受体含量增加。在PHA处理72 h和OKT‐3处理48 h后，细胞结合达到峰值。125i - IGF - I与T细胞膜的亲和交联显示出单个~ 130 kDa的条带，在PHA或OKT - 3处理后增加。添加IGF - I受体单克隆抗体α - IR3可抑制该条带。PHA和OKT‐3均增加了IGF‐I受体mRNA的丰度，分别在20 h和60 h达到峰值。观察到IGF - I受体和β -肌动蛋白mRNA丰度平行增加，与先前的研究一致，表明T细胞活化后肌动蛋白基因表达增加。因此，在PHA刺激后，IGF - I受体mRNA丰度的增加明显先于IGF - I受体含量的增加，但在OKT - 3刺激后，IGF - I受体mRNA丰度的增加紧随IGF - I受体含量的增加。因此，这些研究表明，这两种激活细胞中的IGF - I受体含量主要不是在稳态mRNA水平上调节的。
The biological effects of the IGFs are mediated through interaction with specific cell surface receptors. It has been previously reported that mitogenic activation of T‐lymphocytes by phytohemagglutinin (PHA) is associated with increased IGF‐I receptor content. However, the mechanisms which regulate IGF‐I receptor expression during T‐lymphocyte activation are unknown. To explore further the regulation of IGF‐I receptor expression in T‐cells, we investigated IGF‐I receptor content and mRNA abundance in T‐lymphocytes after stimulation either by PHA or OKT‐3, the latter being a monoclonal antibody directed against the CD‐3 antigen of the T‐cell receptor IGF‐I binding in T‐cells demonstrated increased IGF‐I receptor content after stimulation by both PHA and OKT‐3. Peak binding was induced after 72 h of treatment with PHA and 48 h of treatment with OKT‐3. Affinity cross‐linking of125I‐IGF‐I to T‐cell membranes demonstrated a single ∼ 130 kDa band which was increased after treatment with PHA or OKT‐3. This band was inhibited by the addition of α‐IR3, a monoclonal antibody to the IGF‐I receptor. Both PHA and OKT‐3 increased IGF‐I receptor mRNA abundance with peak increases at 20 h and 60 h, respectively. Parallel increases in IGF‐I receptor and β‐actin mRNA abundance were observed, consistent with previous studies demonstrating increased actin gene expression after T‐cell activation. Thus, the increase in IGF‐I receptor mRNA abundance markedly preceded the increase in IGF‐I receptor content after PHA stimulation, but the increase in IGF‐I receptor mRNA abundance followed the increase in IGF‐I receptor content after OKT‐3. These studies suggest, therefore, that IGF‐I receptor content in both of these activated cells is not regulated primarily at the level of steady state mRNA.