期刊
BIOSCIENCE REPORTS
卷 32, 期 2, 页码 105-112出版社
PORTLAND PRESS LTD
DOI: 10.1042/BSR20110089
关键词
mitogen-activated protein kinase (MAPK); nuclear factor kappa B (NF-kappa B); periodic syndrome; tumour necrosis factor (TNF); tumour necrosis factor receptor-associated periodic syndrome (TRAPS)
资金
- Barts
- London Charitable Foundation
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-kappa B (nuclear factor kappa B) 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.
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