Target intelligence / Profile preview

Toll-like receptors 2, 3, 7, and 8 (TLR2, TLR3, TLR7, TLR8)

Target
TLR2, TLR3, TLR7, TLR8
Molecular classification
Receptor, Pattern-recognition receptor, Innate immune receptor, Type I transmembrane protein
01

Overview

Toll-like receptors 2, 3, 7, and 8 are single-pass transmembrane proteins expressed predominantly in immune cells. Each receptor detects different pathogen-associated molecular patterns: TLR2 recognizes bacterial lipoproteins; TLR3 recognizes double-stranded viral RNA; TLR7 and TLR8 recognize single-stranded viral RNA. Upon ligand binding, they initiate signal transduction through adaptor proteins (MyD88, TRIF), activating NF-κB and IRFs to produce inflammatory cytokines and type I interferons, thereby orchestrating the immune response. Their dysregulation is associated with infectious, inflammatory, and autoimmune diseases, making them important targets for drug development and disease modulation.

Other names
CD282Toll-like receptor familyTLRs
02

Mechanism of action

Agonism (immune stimulation by triggering receptors); Antagonism/inhibition (immune suppression or reduction of excess inflammation); Downstream signaling via MyD88-dependent and TRIF-dependent pathways, leading to NF-κB and interferon production

03

Biological functions

Pathogen recognitionImmune response activation (especially innate immune response)Cytokine productionSignal transductionInflammation regulationBridging innate and adaptive immunity
04

Disease associations

InfectionInflammationAutoimmune diseaseCancerNeurodegenerative diseaseOther diseases linked to inappropriate immune activation
05

Safety considerations

Excessive activation may cause cytokine storm, systemic inflammation, and autoimmunityChronic stimulation implicated in tissue damageOff-target immune effects (e.g., hyperinflammatory diseases)
06

Interacting drugs

Imiquimod (TLR7 agonist)

5 more in the full profile.

07

Biomarkers

Expression levels of TLRs in immune cellsCytokine profiles (e.g., Type I interferons, TNFα, IL-6) following stimulationUpregulation in disease states (autoimmunity, infection, cancer)

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