Subject:
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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:
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Internal Medicine Rheumatology |
Journal title:
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Expert Opinion on Biological Therapy
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Abstract:
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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.
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