Abstract
Acute gout is an auto-inflammatory disease characterized by self-limiting inflammation in response to the deposition of monosodium urate (MSU) crystals in the joints or tissues. Recognition of MSU triggers activation of the NLRP3 inflammasome, release of active interleukin (IL)-1β, and amplification of the inflammatory response by the surrounding tissue followed by recruitment and activation of inflammatory leukocytes. The shutdown of this inflammatory response is linked to a number of regulatory events ranging from crystal coating and apoptotic cell clearance through to pro-inflammatory cytokine regulation and transforming growth factor β1 (TGFβ1) production. This review will highlight mechanisms that limit acute inflammation triggered by MSU crystals and suggests areas for further research.
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