A monoclonal antibody to the T-cell receptor increases IGF-I receptor content in normal T-lymphocytes: Comparison with phytohemagglutinin

✍ Scribed by Klaus K. P. Hartmann; Vincenzo Papa; Eric J. Brown; Ira D. Goldfine; Stephen M. Rosenthal; Thomas G. Baier; Michael Kronenwett

• Publisher: John Wiley and Sons
• Year: 1992
• Tongue: English
• Weight: 467 KB
• Volume: 48
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.240480112

✦ Synopsis

Abstract

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 of ^125^I‐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.