Inflammation in Acute Kidney Injury: Focus on Toll-Like Receptors

Abstract

The molecular mechanisms of acute kidney injury (AKI) remain unclear. AKI is known to be associated with intrarenal and systemic inflammation. The innate immune system plays an important role as a first response to tissue injury. Toll-like receptors (TLRs), the first identified and best studied family of pattern recognition receptors, are key regulators of the inflammatory response and have been associated with many cellular processes activated during AKI. These receptors are expressed on a variety of cell types, including epithelial cells, endothelia, dendritic cells, monocytes/macrophages, and B and T cells. TLRs initiate innate immune responses and shape the subsequent adaptive immune response. Pathogen-associated molecular patterns (PAMPS), which are the conserved microbial motifs, are sensed by these receptors. Increasingly recognized is that endogenous molecules generated during tissue injury and labeled as damage-associated molecular pattern molecules (DAMPs), can also activate pattern recognition receptors