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Blood, Vol. 94 No. 5 (September 1), 1999:
pp. 1782-1789
Enhanced B7-2 Gene Expression by Interferon- in Human Monocytic
Cells Is Controlled Through Transcriptional and Posttranscriptional
Mechanisms
R.E. Curiel,
C.S. Garcia,
S. Rottschafer,
M.C. Bosco, and
I. Espinoza-Delgado
From Department of Medicine and Stanley S. Scott Cancer Center,
Louisiana State University Medical Center, New Orleans, LA; and
Laboratorio di Biologia Molecolare, Instituto Giannina Gaslini, Genova
Quarto, Italy.
B7-2 is a costimulatory molecule expressed on professional
antigen-presenting cells that provides T cells with a critical signal
resulting in T-cell activation. Interferon- (IFN-) enhances B7-2
protein expression in monocytic cells. However, the molecular mechanisms controlling the enhanced expression of B7-2 are poorly understood. Northern blot and flow cytometry analysis revealed that
human monocytes and the human monocytic cell line MonoMac6 (MM6)
constitutively expressed B7-2 mRNA and protein and IFN- treatment
further enhanced the expression of both molecules. The ability of
IFN- to enhance B7-2 mRNA was evident at the dose of 31 U/mL and
reached plateau levels at 500 U/mL. The effects of IFN- on B7-2 mRNA
expression were time dependent and occurred within 3 hours of treatment
and increased through 24 hours. In vitro transcription assays and mRNA
stability experiments showed that IFN- increases both
transcriptional activity and the stability of B7-2 mRNA. Treatment of
MM6 cells with cycloheximide showed that de novo protein synthesis was
not required for the IFN--enhanced expression of B7-2 mRNA.
Overall, these studies show for the first time that IFN--enhanced
expression of B7-2 protein in human monocytic cells is controlled at
the gene level through a dual mechanism involving transcriptional and
posttranscriptional mechanisms.
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