TLR3

Chr 4ADAR

toll like receptor 3

Also known as: CD283, IIAE2, IMD83

TLR3 encodes a Toll-like receptor that recognizes double-stranded RNA from viruses and activates innate immune responses through NF-kappaB and interferon pathways. Mutations cause immunodeficiency with increased susceptibility to viral infections, particularly severe complications from common viruses like HSV and influenza. The gene shows both autosomal dominant and autosomal recessive inheritance patterns depending on the specific variant.

Summary from RefSeq, OMIM, UniProt
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Primary Disease Associations & Inheritance

{HIV1 infection, resistance to}MIM #609423
{Immunodeficiency 83, susceptibility to viral infections}MIM #613002
ADAR
3
Active trials
345
Pubs (1 yr)
51
P/LP submissions
0%
P/LP missense
0.80
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryTLR3
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
51 unique Pathogenic / Likely Pathogenic· 272 VUS of 435 total submissions
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Clinical Trials
3 active or recruiting trials — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.80LOEUF
pLI 0.000
Z-score 2.41
OE 0.53 (0.360.80)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.51Z-score
OE missense 0.93 (0.861.01)
427 obs / 457.9 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.53 (0.360.80)
00.351.4
Missense OE0.93 (0.861.01)
00.61.4
Synonymous OE1.03
01.21.6
LoF obs/exp: 16 / 30.3Missense obs/exp: 427 / 457.9Syn Z: -0.31
DN
0.74top 25%
GOF
0.75top 25%
LOF
0.2386th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). Both the Badonyi & Marsh prediction and the broader genomic evidence point to gain-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median
DNprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

435 submitted variants in ClinVar

Classification Summary

Pathogenic47
Likely Pathogenic4
VUS272
Likely Benign103
Benign3
Conflicting1
47
Pathogenic
4
Likely Pathogenic
272
VUS
103
Likely Benign
3
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
47
0
47
Likely Pathogenic
0
0
4
0
4
VUS
13
230
27
2
272
Likely Benign
0
2
12
89
103
Benign
0
0
3
0
3
Conflicting
1
Total132329391430

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

TLR3 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Literature
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