Abstract
Pathogen recognition receptors (PRRs) are a class of germ line-encoded receptors that recognize pathogen-associated molecular patterns (PAMPs). The activation of PRRs is crucial for the initiation of innate immunity, which plays a key role in first-line defense until more specific adaptive immunity is developed. PRRs differ in the signaling cascades and host responses activated by their engagement and in their tissue distribution. Currently identified PRR families are the Toll-like receptors (TLRs), the C-type lectin receptors (CLRs), the nucleotide-binding oligomerization domain-like receptors (NLRs), the retinoic acid-inducible gene-I-like receptors (RLRs), and the AIM2-like receptor (ALR). The environment of the dental pulp is substantially different from that of other tissues of the body. Dental pulp resides in a low compliance root canal system that limits the expansion of pulpal tissues during inflammatory processes. An understanding of the PRRs in dental pulp is important for immunomodulation and hence for developing therapeutic targets in the field of endodontics. Here we comprehensively review recent finding on the PRRs and the mechanisms by which innate immunity is activated. We focus on the PRRs expressed on dental pulp and periapical tissues and their role in dental pulp inflammation.
Highlights
The innate immune response is the first line of defense against infectious diseases and tissue damage
pattern recognition receptors (PRRs) are classified into five main families: Toll-like receptors (TLRs) and C-type lectin receptors (CLRs), transmembrane proteins found in the plasma membrane, and retinoic acid-inducible gene-I-like receptors (RLRs), AIM2-like receptor (ALR), and the nucleotide-binding oligomerization domain-like receptors (NLRs) proteins located in intracellular compartment [3]
Hirao et al demonstrated that human pulp fibroblasts constitutively express intracellular NOD1 and NOD2 as well as TLR2 and TLR4, and each PRR-specific ligand was upregulated to produce various proinflammatory mediators, suggesting that NODs have a potent influence on proinflammatory responses in dental pulp [16]
Summary
The innate immune response is the first line of defense against infectious diseases and tissue damage. The signal transduction pathways that are activated via PRRs converge on a common set of signaling modules including nuclear factor- (NF-) κB, activator protein-1 (AP-1), and mitogen-activated protein kinase (MAPK). These modules drive the production of Mediators of Inflammation proinflammatory cytokines/chemokines such as interleukin(IL-) 1, tumor necrosis factor- (TNF-) α, and IL-6 [1, 2, 5]. Accumulating evidence of a relationship between bacterial recognition systems and oral disease has focused attention on the role of dental pulp tissues and their associated pathogens in innate immunity. We will describe recent findings concerning the receptors for innate immunity in dental pulp
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