TLRs induce inflammatory gene expression by regulating the activities and expression of signal-dependent transcription factors that include members of the NF-κB, AP-1 and IRF families (Kawai and Akira, 2007). The TLRs play essential roles in innate immune responses to microbial pathogens based on their ability to recognize pathogen-associated molecular patterns (Akira et al., 2006; Medzhitov, 2007). More recently, genetic loss-of-function experiments in mice have shown that TLRs contribute to the pathogenesis of a number of diseases in which inflammation is known to play a pathogenic role, including atherosclerosis, inflammatory bowel disease, and liver fibrosis (Atkinson, 2008). These results are consistent with TLRs being able to signal in response to the generation of endogenously derived ligands, such as components of necrotic cells.
