Mechanisms of uric acid crystal-mediated autoinflammation
Fabio Martinon,
Fabio Martinon
Department of Immunology and Infectious Diseases, Harvard School of Public Health Boston, MA, USA.
Search for more papers by this authorFabio Martinon,
Fabio Martinon
Department of Immunology and Infectious Diseases, Harvard School of Public Health Boston, MA, USA.
Search for more papers by this authorFabio Martinon
Department of Immunology and Infectious DiseasesHarvard School of Public Health651 Huntington AveBoston, MA 02115, USATel.: +1 617 432 4689Fax: +1 617 432 0084e-mail: [email protected]
Abstract
Summary: Gout is an arthritis characterized by elevated uric acid in the bloodstream. In this condition, crystals of uric acid are formed and accumulate in the synovial fluids. Crystal deposition leads to acute inflammation, which is associated with the spontaneous resolution of the disease. Recent studies have led to significant advances in the understanding of the basic biology of crystal-mediated inflammation. Uric acid has been identified as a danger signal that triggers a cytosolic sensor, the inflammasome. This signaling platform is required for the activation of interleukin-1, a cytokine that is critical to the initiation of acute inflammation in gout. Importantly, both molecular and pathological evidence support the notion that gout is a prototypical member of the growing family of autoinflammatory diseases. This review discusses the role of the inflammasome in gout and the emerging new therapeutic strategies aimed at controlling inflammation in crystal arthritis.
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