Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) are two major forms of innate immune sensors which provide immediate responses against pathogenic invasion, tissue injury and stress conditions. Both the TLRs and NLRs families of receptors are activated through the recognition of both conserved microbial structures, called pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). However, unlike membrane-bound TLRs that sense PAMPs or DAMPs on the cell surface or within endosomes, NLRs recognize microbial molecules or DAMPs in the host cytosol. Activation of these receptors induces the recruitment of innate immune cells, which initiates tissue repair processing and adaptive immune activation. Abnormalities in any of these innate sensor-mediated processes may cause excessive inflammation due to either hyper-responsive innate immune signaling or sustained compensatory adaptive immune activation.
