An Overview of Pathogen Recognition Receptors for Innate Immunity in Dental Pulp

Figure 1

Schematic overview of TLR and NLR signaling pathways. PAMPs and DAMPs are recognized by PRRs. Heterodimer of TLR1/6+TLR2, TLR4, and endosomal TLR3 activate TRIF pathway, followed by induction of IRF and NF-κB. TLR5 and endosomal TLR9 and TLR7 activate MyD88 pathway, followed by activation of MAPK, NF-κB, and IRF7. NOD1 and NOD2 are cytoplasmic PRRs, and they trigger NF-κB, and NALP3 inflammasome recruits and activates caspase-1 pathway. DAMP: damage-associated molecular patterns; IRF: IFN-regulatory factor; MAPK; mitogen-activated protein kinase; MyD88; myeloid differentiation primary-response gene 88; NF-κB: nuclear factor-κB; NALP3: NACHT, LRR, and pyrin domain containing protein 3; NOD: nucleotide-binding oligomerization domain; NLR: NOD-like receptor; PAMP: pathogen-associated molecular patterns; TLR: Toll-like receptor; TRIF: Toll/IL-1R (TIR) domain containing adaptor protein inducing IFN-β.