IL27RA

Chr 19AR

interleukin 27 receptor subunit alpha

Also known as: CRL1, IL-27RA, IL27R, TCCR, WSX1, zcytor1

The IL27RA protein functions as a receptor for IL-27 and requires IL6ST/GP130 for signal transduction, playing a key role in regulating Th1-type immune responses and innate defense mechanisms. Autosomal recessive mutations cause Immunodeficiency 134, which is characterized by specific susceptibility to Epstein-Barr virus infections. This gene is extremely intolerant to loss-of-function variants (pLI near 0), indicating that complete loss of protein function is likely pathogenic.

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

Immunodeficiency 134 (Epstein-Barr virus-specific)MIM #621405
AR
0
Active trials
9
Pubs (1 yr)
16
P/LP submissions
0%
P/LP missense
0.90
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryIL27RA
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
16 unique Pathogenic / Likely Pathogenic· 90 VUS of 138 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.90LOEUF
pLI 0.000
Z-score 2.03
OE 0.64 (0.460.90)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.12Z-score
OE missense 0.84 (0.760.92)
310 obs / 370.6 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.64 (0.460.90)
00.351.4
Missense OE0.84 (0.760.92)
00.61.4
Synonymous OE0.88
01.21.6
LoF obs/exp: 24 / 37.4Missense obs/exp: 310 / 370.6Syn Z: 1.14
DN
0.6746th %ile
GOF
0.75top 25%
LOF
0.2582th %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

138 submitted variants in ClinVar

Classification Summary

Pathogenic15
Likely Pathogenic1
VUS90
Likely Benign10
Benign4
Conflicting3
15
Pathogenic
1
Likely Pathogenic
90
VUS
10
Likely Benign
4
Benign
3
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
15
0
15
Likely Pathogenic
0
0
1
0
1
VUS
0
87
3
0
90
Likely Benign
0
8
0
2
10
Benign
0
1
1
2
4
Conflicting
3
Total096204123

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

View in ClinVar →

Protein Context — Lollipop Plot

IL27RA · 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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