The role of NLRs and TLRs in the activation of the inflammasome.

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Title:	The role of NLRs and TLRs in the activation of the inflammasome.
Author(s):	Netea, M.G. ; Veerdonk, F.L. van de ; Kullberg, B.J. ; Meer, J.W.M. van der ; Joosten, L.A.B.
Publication year:	2008
Source:	Expert Opinion on Biological Therapy, vol. 8, iss. 12, (2008), pp. 1867-1872
ISSN:	1471-2598
DOI:	https://doi.org/10.1517/14712590802494212
Publication type:	Article / Letter to editor
Please use this identifier to cite or link to this item : https://hdl.handle.net/2066/70654
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Subject:	DCN 1: Perception and Action N4i 1: Pathogenesis and modulation of inflammation N4i 2: Invasive mycoses and compromised host N4i 4: Auto-immunity, transplantation and immunotherapy NCMLS 1: Immunity, infection and tissue repair NCMLS 1: Infection and autoimmunity UMCN 4.1: Microbial pathogenesis and host defense UMCN 4.2: Chronic inflammation and autoimmunity
Organization:	Internal Medicine Rheumatology
Journal title:	Expert Opinion on Biological Therapy
Volume:	vol. 8
Issue:	iss. 12
Page start:	p. 1867
Page end:	p. 1872
Abstract:	BACKGROUND: Interleukin-1 beta is one of the most important pro-inflammatory cytokines. In contrast to other cytokines, activation of IL-1 beta requires processing from an inactive precursor by the cysteine protease caspase-1. Caspase-1 forms a protein platform called the inflammasome, together with proteins of the nucleotide-binding oligomerization domain-like receptor (NLR) family. OBJECTIVE/METHODS: A review of literature investigating the stimulation of IL-1 beta production by microbial pathogens and their components. RESULTS/CONCLUSIONS: To produce IL-1 beta, macrophages need a double stimulation with Toll like receptor (TLR) ligands that induce gene transcription, and NLR agonists (such as ATP or muramyl dipeptide (MDP)) that activate the inflammasome. Monocytes can release active IL-1 beta upon stimulation with TLR ligands alone. This probably represents an adaptation of each cell type to its environment.