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Toll-like receptors (TLRs) and NOD-like receptors (NLRs) are two major classes of pattern recognition receptors (PRRs) that detect conserved molecules associated with pathogens (PAMPs) and endogenous danger signals (DAMPs), initiating innate immune responses. TLRs are single-pass transmembrane proteins, typically expressed on the cell surface or endosomal membranes, responsible for the recognition of a broad range of microbial molecules and activating signaling cascades leading to inflammation, cytokine production, and modulation of adaptive immunity. NLRs are cytosolic receptors that sense intracellular danger signals, including microbial components and metabolic stress, and can oligomerize to form inflammasomes which mediate maturation of inflammatory cytokines such as IL-1β and IL-18. Both receptor families are implicated in numerous diseases when dysregulated, including infections, chronic inflammatory diseases, autoimmune disorders, and cancer. The designation "Toll-like receptors and NOD-like receptors" refers to two large families of related but distinct receptors, not a single molecule or canonical target. Each family comprises multiple subtypes (e.g., TLR1–TLR10, NOD1, NOD2, NLRP3, etc.), and each should ideally be considered separately in structured target databases. Therefore, this entry is overly broad and not specific to a single molecule/receptor; use with caution for structured data purposes.
Agonists: stimulate receptor to induce immune activation, cytokine release. Antagonists/inhibitors: block receptor activation to reduce inflammation or autoimmunity. Modulation of inflammasome formation (NLRs): block or alter IL-1β/IL-18 release.
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