Role of a novel pathogen sensor in the pathophysiology of acute renal failure

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Accumulating evidence suggests that pathogen sensors such as TLRs and C-type lectin families are capable of sensing endogenous ligands released from damaged and stressed cells and tissues, thereby inducing sterile inflammation. Here we demonstrate that macrophage-inducible C-typelectin (Mince) is involved in the pathophysiology of renal ischemia-reperfusion injury, an experimental model of acute renal failure. Our data also suggest that Mincle is mainly expressed in proinflammatory macrophages that infiltrate into the damaged kidney.