UNSPECIFIED. (2004) Nuclear factor-kappa B does not mediate the inhibitory effects of dexamethasone on granulocyte-macrophage colony-stimulating factor expression. IMMUNOLOGY, 111 (4). pp. 430-434. ISSN 0019-2805

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Abstract

Human granulocyte-macrophage colony-stimulating factor (GM-CSF) reporter constructs containing up to 3.3 kb of upstream promoter sequence were transiently transfected into both Jurkat and HUT78 human T-cell lines. In Jurkat cells, stimulation with phorbol 12-myristate 13-acetate (PMA) plus phytohemaglutinin (PHA) produced robust increases in reporter activity, whereas HUT78 cells showed low levels of reporter induction attributable to constitutive nuclear factor (NF)-kappaB activity. Following mutation of either the proximal NF-kappaB site (-85/-76) or the activator protein1 (AP-1) motif within the conserved lymphokine element 0 (CLE0) site (-54/-31), reporter activity was markedly reduced in both cell lines. Despite this dependence on NF-kappaB and CLE0/AP-1, GM-CSF reporter activity was unaffected by dexamethasone in either cell line. Similarly, an NF-kappaB-dependent reporter was also not repressed by dexamethasone, yet GM-CSF release from HUT78 T cells was inhibited. These data therefore confirm a critical role for both NF-kappaB and CLE0 sites in GM-CSF promoter activation and indicate that NF-kappaB may not mediate glucocorticoid-dependent repression of GM-CSF in these cells.

Item Type:	Journal Article
Subjects:	Q Science > QR Microbiology > QR180 Immunology
Journal or Publication Title:	IMMUNOLOGY
Publisher:	BLACKWELL PUBLISHING LTD
ISSN:	0019-2805
Date:	April 2004
Volume:	111
Number:	4
Number of Pages:	5
Page Range:	pp. 430-434
Identification Number:	10.1111/j.1365-2567.2004.01833.x
Publication Status:	Published
URI:	http://wrap.warwick.ac.uk/id/eprint/8579

Data sourced from Thomson Reuters' Web of Knowledge

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