TNFRSF18

Chr 1

TNF receptor superfamily member 18

Also known as: AITR, CD357, ENERGEN, GITR, GITR-D

The protein is a TNF receptor superfamily member that regulates T-cell activation, immune tolerance through regulatory T cells, and T-cell receptor-mediated cell death via NF-kappa-B signaling. This gene is extremely intolerant to loss-of-function mutations (pLI near 1.0), indicating that haploinsufficiency likely causes severe disease, though specific clinical phenotypes associated with TNFRSF18 mutations have not been well-established in humans. Given its critical role in immune regulation, mutations would be expected to cause primary immunodeficiency or autoimmune disorders.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
18
Pubs (1 yr)
137
P/LP submissions
0%
P/LP missense
1.88
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryTNFRSF18
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
130 unique Pathogenic / Likely Pathogenic· 88 VUS of 246 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.88LOEUF
pLI 0.000
Z-score -0.60
OE 1.26 (0.721.88)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.57Z-score
OE missense 1.13 (1.001.28)
175 obs / 155.1 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE1.26 (0.721.88)
00.351.4
Missense OE1.13 (1.001.28)
00.61.4
Synonymous OE1.13
01.21.6
LoF obs/exp: 8 / 6.4Missense obs/exp: 175 / 155.1Syn Z: -0.87
DN
0.6162th %ile
GOF
0.6932th %ile
LOF
0.2969th %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

246 submitted variants in ClinVar

Classification Summary

Pathogenic124
Likely Pathogenic6
VUS88
Likely Benign20
Benign1
124
Pathogenic
6
Likely Pathogenic
88
VUS
20
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
124
0
124
Likely Pathogenic
0
0
6
0
6
VUS
0
65
23
0
88
Likely Benign
0
15
1
4
20
Benign
0
0
1
0
1
Total0801554239

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

View in ClinVar →

Protein Context — Lollipop Plot

TNFRSF18 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
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