The induction of proinflammatory factors in DCs requires the involvement of TLR2 and TLR4, and specific intercellular adhesion molecule-3-grabbing non-integrin (SIGN) on DCs captures nonintegrin 1, which interacts with TLR4 to regulate the inflammatory response of renal tubular epithelial cells and is involved in the pathogenesis of AKI (95, 96). This evidence concerns the gene TLR4 and acute kidney injury.