Post-transcriptional regulation of pro-inflammatory gene expression.
The cytokine tumour necrosis factor (TNF)alpha is a vital mediator of the innate immune response, and a pleiotropic regulator of cellular function. Its involvement in rheumatoid arthritis is illustrated by the clinical benefits of TNF alpha blockade. Post-transcriptional regulation (the control of mRNA stability and translation) appears to play a critical role in the regulation of TNF alpha expression by mitogen activated protein kinase signal transduction pathways and by anti-inflammatory agents. The aim of this article is to review some recent advances in our understanding of these processes, and to speculate on mechanisms of regulation of TNF alpha and other pro-inflammatory genes.
Clark
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Kennedy Institute of Rheumatology, Imperial College School of Medicine, London, UK. a.clark@cxwms.ac.uk
D006801:Humans; D012323:RNA Processing, Post-Transcriptional / Q000276:immunology*; D012216:Rheumatic Diseases / Q000235:genetics* / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics* / Q000276:immunology*
D014409:Tumor Necrosis Factor-alpha