Tubular epithelial cells of the kidney are among the nonimmune cells that express TLR1, TLR1-2, TLR1-3, TLR1-4, and TLR1-6, suggesting that these TLR might contribute to the activation of immune responses in tubulointerstitial injury (45) . In addition, receptors such as TLR4, TLR2, CD91 and the receptor for the advanced glycation end-products (RAGE), allow leukocytes and renal cells to recognize molecules released by injured cells. These receptors are sentinels for tissue necrosis (46) . Upon stimulation with LPS in renal infection or other endogenous ligands from necrotic tubular cells, the activated TLR4 has been shown to specifically stimulate the NF-κB pathway in response to oxidative stress (47) . Furthermore, TLR4 activation on tubular epithelial cells and circulating immune cells leads to secretion of cytokines and chemokines that either directly or indirectly contributes to renal injury.