Journal
NEPHROLOGY DIALYSIS TRANSPLANTATION
Volume 29, Issue 1, Pages 41-48Publisher
OXFORD UNIV PRESS
DOI: 10.1093/ndt/gft332
Keywords
crystal nephropathy; dendritic cells; glomerulonephritis; macrophages; tubular injury
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Funding
- Deutsche Forschungsgemeinschaft [AN372/9-2, AN372]
- Else Kroner-Fresenius Stiftung [P22-09/A14-09]
- European Comission (REDDSTAR)
- [GRK1202]
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NLRP-3 inflammasome is one of several intracellular danger recognition platforms that integrates infectious or non-infectious types of danger into the expression of pro-inflammatory cytokines to set-up inflammation for danger control. NLRP3 activation induces three types of caspase-1-mediated responses: secretion of IL-1beta, secretion of IL-18 and a programmed form of cell death, referred to as pyroptosis. Similar to the well-documented impact of Toll-like receptor-driven danger signalling in kidney disease, evolving data now suggest a similar involvement of the NLRP3 inflammasome in renal inflammation. Here, we discuss the accumulating data on NLRP3 in the kidney: its IL-1beta and IL-18-dependent canonical effects and the current evidence for its non-canonical effects, e.g. in tumor growth factor (TGF)-beta signalling, epithelial-mesenchymal transition and fibrosis. Research in this area will certainly uncover yet unknown aspects of danger signalling in the kidney and how it drives renal inflammation and immunopathology.
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