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- (IFN-) 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- 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- 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- augmented monocyte chemotactic protein-1 expression in the same cell preparations. PTX3 protein secretion by activated monocytes is also suppressed by exposure to IFN-. Altogether, these data identify a negative pathway of regulation mediated by IFN-, which may occur under inflammatory conditions.
Interferon-gamma inhibits expression of the long pentraxin PTX3 in human monocytes / N. Polentarutti, G. Picardi, A. Basile, S. Cenzuales, A. Rivolta, C. Matteucci, G. Peri, A. Mantovani, M. Introna. - In: EUROPEAN JOURNAL OF IMMUNOLOGY. - ISSN 0014-2980. - 28:2(1998 Feb), pp. 496-501. [10.1002/(SICI)1521-4141(199802)28:02<496::AID-IMMU496>3.0.CO;2-V]
Interferon-gamma inhibits expression of the long pentraxin PTX3 in human monocytes
A. Basile;A. MantovaniPenultimo
;
1998
Abstract
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- (IFN-) 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- 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- 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- augmented monocyte chemotactic protein-1 expression in the same cell preparations. PTX3 protein secretion by activated monocytes is also suppressed by exposure to IFN-. Altogether, these data identify a negative pathway of regulation mediated by IFN-, which may occur under inflammatory conditions.Pubblicazioni consigliate
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