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Biosci Rep. 2012 Apr 1;32(2):105-12. doi: 10.1042/BSR20110089.

Tumour necrosis factor receptor trafficking dysfunction opens the TRAPS door to pro-inflammatory cytokine secretion.

Author information

1
Centre for Diabetes, The Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Whitechapel, London E1 2AT, UK. M.D.Turner@qmul.ac.uk

Abstract

Cytokines are secreted from macrophages and other cells of the immune system in response to pathogens. Additionally, in autoinflammatory diseases cytokine secretion occurs in the absence of pathogenic stimuli. In the case of TRAPS [TNFR (tumour necrosis factor receptor)-associated periodic syndrome], inflammatory episodes result from mutations in the TNFRSF1A gene that encodes TNFR1. This work remains controversial, however, with at least three distinct separate mechanisms of receptor dysfunction having been proposed. Central to these hypotheses are the NF-κB (nuclear factor κB) and MAPK (mitogen-activated protein kinase) families of transcriptional activators that are able to up-regulate expression of a number of genes, including pro-inflammatory cytokines. The present review examines each proposed mechanism of TNFR1 dysfunction, and addresses how these processes might ultimately impact upon cytokine secretion and disease pathophysiology.

PMID:
22115362
PMCID:
PMC3204872
DOI:
10.1042/BSR20110089
[Indexed for MEDLINE]
Free PMC Article
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