TY - JOUR
T1 - Interferon-γ inhibits expression of the long pentraxin PTX3 in human monocytes
AU - Polentarutti, Nadia
AU - Picardi, Giuseppina
AU - Basile, Andrea
AU - Cenzuales, Salvatore
AU - Rivolta, Attilio
AU - Matteucci, Cristian
AU - Peri, Giuseppe
AU - Mantovani, Alberto
AU - Introna, Martino
PY - 1998/2
Y1 - 1998/2
N2 - PTX3 is a prototypic long pentraxin expressed by various cell types, most prominently monocytes and endothelial cells, in response to interleukin-1 (IL-1), tumor necrosis factor (TNF) and bacterial products. In the present report, we show that interferon-γ (IFN-γ) inhibits the expression of the PTX3 gene induced by exposure to IL-1, TNF or lipopolysaccharide in human monocytes. This effect is dose dependent and observable when IFN-γ is added from 24 h before up to 3 h after the addition of IL-1. While the time course of the IL-1-induced PTX3 mRNA expression is not affected, IFN-γ reduces the stability of the PTX3 mRNA as well as its transcription. The inhibition of PTX3 expression is restricted to monocytes in that no inhibition occurs in cytokine-stimulated fibroblasts and endothelial cells. Under the same conditions, as expected, IFN-γ augmented monocyte chemotactic protein-1 expression in the same cell preparations. PTX3 protein secretion by activated monocytes is also suppressed by exposure to IFN-γ. Altogether, these data identify a negative pathway of regulation mediated by IFN-γ, which may occur under inflammatory conditions.
AB - PTX3 is a prototypic long pentraxin expressed by various cell types, most prominently monocytes and endothelial cells, in response to interleukin-1 (IL-1), tumor necrosis factor (TNF) and bacterial products. In the present report, we show that interferon-γ (IFN-γ) inhibits the expression of the PTX3 gene induced by exposure to IL-1, TNF or lipopolysaccharide in human monocytes. This effect is dose dependent and observable when IFN-γ is added from 24 h before up to 3 h after the addition of IL-1. While the time course of the IL-1-induced PTX3 mRNA expression is not affected, IFN-γ reduces the stability of the PTX3 mRNA as well as its transcription. The inhibition of PTX3 expression is restricted to monocytes in that no inhibition occurs in cytokine-stimulated fibroblasts and endothelial cells. Under the same conditions, as expected, IFN-γ augmented monocyte chemotactic protein-1 expression in the same cell preparations. PTX3 protein secretion by activated monocytes is also suppressed by exposure to IFN-γ. Altogether, these data identify a negative pathway of regulation mediated by IFN-γ, which may occur under inflammatory conditions.
KW - Acute-phase reactants
KW - Gene regulation
KW - Human
KW - Inflammation
KW - Monocyte
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U2 - 10.1002/(SICI)1521-4141(199802)28:02<496::AID-IMMU496>3.0.CO;2-V
DO - 10.1002/(SICI)1521-4141(199802)28:02<496::AID-IMMU496>3.0.CO;2-V
M3 - Article
C2 - 9521058
AN - SCOPUS:0031938412
VL - 28
SP - 496
EP - 501
JO - European Journal of Immunology
JF - European Journal of Immunology
SN - 0014-2980
IS - 2
ER -