TNFRSF4

Chr 1AR

TNF receptor superfamily member 4

Also known as: ACT35, CD134, IMD16, OX40, TXGP1L

The TNFRSF4 protein is a TNF receptor superfamily member that serves as a costimulatory receptor for T-cell activation and promotes T-cell survival by suppressing apoptosis through NF-kappaB signaling. Mutations cause autosomal recessive immunodeficiency 16, characterized by defective T-cell responses and impaired T cell-dependent B cell function. The gene shows low constraint against loss-of-function variants (pLI 0.0001, LOEUF 1.32), consistent with the recessive inheritance pattern requiring biallelic mutations for disease manifestation.

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

?Immunodeficiency 16MIM #615593
AR
3
Active trials
39
Pubs (1 yr)
116
P/LP submissions
0%
P/LP missense
1.32
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryTNFRSF4
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Gene-Disease Validity (ClinGen)
combined immunodeficiency due to OX40 deficiency · ARLimited

Limited evidence — not for standalone diagnostic reporting

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
110 unique Pathogenic / Likely Pathogenic· 212 VUS of 499 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
1.32LOEUF
pLI 0.000
Z-score 0.86
OE 0.71 (0.401.32)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.62Z-score
OE missense 0.86 (0.750.99)
142 obs / 164.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.71 (0.401.32)
00.351.4
Missense OE0.86 (0.750.99)
00.61.4
Synonymous OE0.98
01.21.6
LoF obs/exp: 7 / 9.9Missense obs/exp: 142 / 164.5Syn Z: 0.16
DN
0.7326th %ile
GOF
0.76top 25%
LOF
0.2776th %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

499 submitted variants in ClinVar

Classification Summary

Pathogenic104
Likely Pathogenic6
VUS212
Likely Benign148
Benign19
Conflicting5
104
Pathogenic
6
Likely Pathogenic
212
VUS
148
Likely Benign
19
Benign
5
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
104
0
104
Likely Pathogenic
0
0
6
0
6
VUS
16
149
43
4
212
Likely Benign
1
8
56
83
148
Benign
0
1
11
7
19
Conflicting
5
Total1715822094494

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

View in ClinVar →

Protein Context — Lollipop Plot

TNFRSF4 · 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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