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Transcription of T cell antigen receptor genes is induced by protein kinase C activation

Lindsten, T.; June, C.H.; Thompson, C.B.

Journal of Immunology 141(5): 1769-1774

1988

ISSN/ISBN: 0022-1767
PMID: 3261760
Document Number: 310594
The regulation of expression of the TCR-.alpha. and -.beta. genes was studied in the human T cell tumor line Jurkat. Treatment of the cells with PMA was shown to decrease the surface expression of the TCR-.alpha./.beta./CD3 complex. Subsequent to PMA-induced modulation of the TCR/CD3 complex, increases in the mRNA levels of both the TCR-.alpha. and -.beta. gene were observed reacing a maximum 12 h after stimulation. Other T cell activators were also examined for their ability to increase TCR-.alpha. and -.beta. mRNA expression. Only agents that activate protein kinase C were shown to induce expression of the TCR-.alpha. and -.beta. genes. The observed increases in TCR-.alpha. and -.beta. gene mRNA levels were not the result of a uniquely derived Jurkat subline. Similar inductions of TCR-.alpha. and -.beta. mRNA levels were observed in an independently maintained Jurkat cell line. In both cell lines, elevations of TCR gene expression was accompanied by a decline in the expression of the c-myc proto-oncogene. PMA induction of TCR-.alpha. and -.beta. mRNA was shown to occur in the presence of the protein synthesis inhibitor cycloheximide. The 1.6-kb TCR-.alpha. and the 1.0-kb D.beta.J.beta.C.beta. TCR-.beta. gene trascripts were fully induced in the presence of cycloheximide, whereas the 1.3-kb V.beta.D.beta.J.beta.C.beta. transcript was only partly induced in the presence of cycloheximide. Run-on transcription assays demonstrated that the increase in TCR-.alpha. and -.beta. mRNA levels could be entirely accounted for by increase in the transcription rate of both gene after PMA induction. Thus, in summary, protein kinase C stimulation leads to TCR-.alpha./.beta. modulation in Jurkat cells and an increase in steady state TCR-.alpha. and -.beta. mRNA levels as a result of transcriptional activation of both genes.

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