T cell CD7 mRNA expression is regulated by both transcriptional and post-transcriptional mechanisms.
The CD7 molecule is a 40 kDa member of the Ig superfamily that is acquired early in human T cell ontogeny. Because of the putative three-dimensional structure of CD7 and its presence on T cell precursors, it has been postulated that CD7 serves as an adhesion molecule that facilitates early T cell maturation. Ligand binding to CD7 on mature peripheral blood (PB) T cells has been reported to deliver a co-mitogenic signal with CD3 mAb for T cell triggering. In previous work, we found that CD7 was upregulated on PB T cells following a non-mitogenic ionomycin-induced transmembrane calcium flux, which induced new T cell CD7 transcription without affecting CD7 mRNA stability. In this report, we have studied the upregulation of CD7 expression on PB T cells following stimulation by ionomycin, phytohemagglutinin (PHA), and CD3 mAb. PHA prolonged T cell CD7 mRNA stability without affecting CD7 transcription, while stimulation of PB T cells with CD3 mAb both increased T cell CD7 transcription and prolonged CD7 mRNA stability. Experiments with cycloheximide demonstrated superinduction of T cell CD7 mRNA and showed that new protein synthesis was not required for ionomycin-induced upregulation of T cell CD7 expression. Cyclosporin A inhibited ionomycin-induced T cell CD7 upregulation at the level of CD7 mRNA transcription and elongation. These data demonstrate that ionomycin, PHA, and CD3 mAb act via different mechanisms to increase T cell CD7 expression, and that both transcriptional and post-transcriptional mechanisms are used to modify CD7 mRNA levels.
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