Renal inflammation is a universal response to infectious and noninfectious triggers. Sensors
of the innate immune system, such as Toll-like receptors or RIG-like receptors, provide
danger recognition platforms on renal cells that integrate and translate the diverse triggers of
renal inflammation by inducing cell activation and the secretion of proinflammatory cytokines
and chemokines. As a new entry, the inflammasome-forming NLR genes integrate various
danger signals into caspase-1-activating platforms that regulate the processing and …