Elsevier

Kidney International

Volume 84, Issue 2, August 2013, Pages 225-228
Kidney International

Commentary
NOD-like and Toll-like receptors or inflammasomes contribute to kidney disease in a canonical and a non-canonical manner

https://doi.org/10.1038/ki.2013.122Get rights and content
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Tissue remodeling in kidney disease involves sterile inflammation, because tissue necrosis, in acute kidney injury, produces endogenous agonists to innate pattern recognition receptors that trigger innate immunity. In chronic kidney disease, however, a functional role of such pattern recognition receptors is questionable. Here we summarize and discuss the current evidence on a potential contribution of canonical and non-canonical pattern recognition receptor signaling in chronic kidney disease.

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The authors declared no competing interest.

Note added in proof

Upon acceptance of this manuscript Sokolovska et al. reported that NLRP3/ASC/caspase-1 induce NADPH oxidase NOX2 to enhance host defense independent of IL-1β and IL-18, which represents a previously unknown non-canonical function of the NLRP3 inflammasome (Sokolovska A, Becker CE, Ip WK et al. Activation of caspase-1 by the NLRP3 inflammasome regulates the NADPH oxidase NOX2 to control phagosome function. Nat Immunol 2013; 14:543-553).