Protein / target

Toll-like receptor 3

Encoded byTLR3O15455Homo sapiensSwiss-Prot

UniProt: O15455 Ensembl: ENSG00000164342 HGNC: HGNC:11849 NCBI Gene: 7098

Clinical-stage

Therapeutic maturity

Clinical candidates

Small-molecule tractable

Druggability

High-Quality Ligand

Research papers

Protein at a glance

Biological role

Transmembrane signaling receptor

Strongest disease association

Hypothyroidism

Via encoding gene TLR3 · Genetic evidence · score 0.94

Therapeutic position

Clinically advancing target

Research activity

Emerging research

4 papers · latest 2020

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Key component of innate and adaptive immunity.

View complete UniProt function annotation

Key component of innate and adaptive immunity. TLRs (Toll-like receptors) control host immune response against pathogens through recognition of molecular patterns specific to microorganisms. TLR3 is a nucleotide-sensing TLR which is activated by double-stranded RNA, a sign of viral infection. Acts via the adapter TRIF/TICAM1, leading to NF-kappa-B activation, IRF3 nuclear translocation, cytokine secretion and the inflammatory response

Subcellular location

Endoplasmic reticulum membraneEndosome membraneEarly endosome

Domains and Gene Ontology detail (51)

Domains & features

LRRNTLRRCTTIR

Gene Ontology

Ccytoplasm
Cearly endosome
Cendolysosome membrane
Cendoplasmic reticulum membrane
Cendosome membrane
CGolgi membrane
Clysosomal membrane
Cmembrane
Cplasma membrane
Fdouble-stranded RNA binding
Fidentical protein binding
Fpattern recognition receptor activity

904 aa · 104 kDa · 2 isoforms

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Immune signallingUniProt · GOTranscriptional regulationGO

View supporting evidence

Immune signalling

·Key component of innate and adaptive immunity. TLRs (Toll-like receptors) control host i…
·inflammatory response to wounding
·innate immune response
·positive regulation of cytokine production involved in inflammatory response

Transcriptional regulation

·positive regulation of gene expression
·positive regulation of transcription by RNA polymerase II

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene TLR3

Gene-level evidence surfaced through the gene TLR3that encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Hypothyroidism

0.94Well supported

Genetic evidence dominant · Open Targets 0.57

Thyroid Diseases

0.89Well supported

Genetic evidence dominant · Open Targets 0.54

Hashimoto's Disease

0.75Well supported

Genetic evidence dominant · Open Targets 0.46

Myxedema

0.75Moderately supported

Genetic evidence dominant · Open Targets 0.46

Autoimmune Diseases

0.61Moderately supported

Genetic evidence dominant · Open Targets 0.37

View evidence synthesis (5)

HypothyroidismWell supported

0.94

agreement 0.81–1.00

Genetic100%Literature1%

Open Targets aggregate 0.57 · 2 independent evidence families

Thyroid DiseasesWell supported

0.89

agreement 0.75–1.00

Genetic98%Literature2%

Open Targets aggregate 0.54 · 2 independent evidence families

Hashimoto's DiseaseWell supported

0.75

agreement 0.61–0.89

Genetic98%Literature2%

Open Targets aggregate 0.46 · 2 independent evidence families

MyxedemaModerately supported

0.75

agreement 0.63–0.87

Genetic100%

Open Targets aggregate 0.46 · 1 independent evidence family

Autoimmune DiseasesModerately supported

0.61

agreement 0.47–0.75

Genetic95%Literature5%

Open Targets aggregate 0.37 · 2 independent evidence families

The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations

Hypothyroidism0.57

Thyroid Diseases0.54

Hashimoto's Disease0.46

Myxedema0.46

Immunologic Deficiency Syndromes0.37

Autoimmune Diseases0.37

Thyroiditis, Autoimmune0.37

Basal cell carcinoma0.36

Drug development

3 compounds recorded · 3 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines.

View all recorded compounds (3)

RINTATOLIMODPhase 3

BEVASIRANIBPhase 3

BEVASIRANIB SODIUMPhase 3

Open Targets known-drugs universe. Drug name and highest clinical stage only — the disease relationship is NOT read from this slice (it carries trial-context noise); approved indications come from the canonical graph above.

Tractability

Small molecules — Emerging

Feasibility evidence (high-quality ligand and druggable family) — no clinical-stage drug of this modality recorded.

Antibodies — Emerging

Feasibility evidence (go cc high conf and uniprot loc med conf) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

Feasibility evidence (uniprot ubiquitination and small molecule binder) — no clinical-stage drug of this modality recorded.

Other modalities — Strong

Advanced Clinical support this modality.

View underlying tractability evidence (8)

SM · High-Quality LigandSM · Druggable FamilyAB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMMPR · UniProt UbiquitinationPR · Small Molecule BinderOC · Advanced Clinical

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

Aspirin-Exacerbated Respiratory DiseaseClinPGx

Terms indexed against this target in Open Targets' safety data, with their datasource. These are annotations, not causal claims: the direction of effect (whether activation or inhibition is implicated), species and evidence strength are not captured here, so an entry does not mean that modulating this target is known to cause that condition.